C2 Forensic Medicine [608266]
CAMELIA LIANA BUHA Ș
FORENSIC MEDICINE
COURSE MATERIAL FOR STUDENTS
ISBN 978 – 606 – 10 – 1540 – 5
2
Table of Contents
CHAPTER 1: INTRODUCTION TO FORENSIC MEDICINE …………………………………… 5
1.1. General aspect. Definition. History. ………………………………………………………………… 5
1.2. Medico Legal Thanatology …………………………………………………………………………….. 6
1.3. Medico-legal Cases……………………………………………………………………………………… 11
1.4. Forensic exam on cadaver and Forensic Autopsy ……………………………………………. 12
1.5. Forensic exam report …………………………………………………………………………………… 14
CHAPTER 2: SUDDEN DEATH …………………………………………………………………………… 16
2.1. Definitions …………………………………………………………………………………………………. 16
2.2. Sudden death in adult age …………………………………………………………………………….. 16
2.2.1. Sudden death from cardiac diseases ………………………………………………………… 16
2.2.2. Sudden death caused by respiratory system disorders………………………………… 19
2.2.3. Sudden death caused by central nervous system disorders …………………………. 20
2.2.4. Sudden death caused by digestive system disorders ………………………………….. 21
2.2.5. Sudden death from the genitor – urinary system………………………………………… 22
2.3. Sudden infant death syndrome (SIDS) …………………………………………………………… 22
CHAPTER 3: EXAMINATION OF ALIVE PERSONS ……………………………………………. 23
3.1. General assessment ……………………………………………………………………………………… 23
3.2. Forensic Certificate……………………………………………………………………………………… 24
CHAPTER 4: DEATH DUE TO MECHANICAL AGENTS – THE PATHOLOGY OF
WOUNDS ……………………………………………………………………………………………………………. 27
4.1. Definition and classification of injuries …………………………………………………………. 27
4.2. Types of injuries …………………………………………………………………………………………. 28
4.2.1. Abrasions (GRAZES/SCRATCHES) ……………………………………………………… 28
4.2.2. Bruises (Contusions) …………………………………………………………………………….. 29
4.2.3. Lacerations…………………………………………………………………………………………… 30
4.2.4. Wounds ……………………………………………………………………………………………….. 31
CHAPTER 5: GUNSHOT WOUNDS …………………………………………………………………….. 33
5.1. The mechanics of the missile injury ………………………………………………………………. 33
5.2. Types of weapon …………………………………………………………………………………………. 34
5.3. Wounds ……………………………………………………………………………………………………… 34
5.4. Firearm damage to internal organs ………………………………………………………………… 40
5.5. Shooting distance estimation ………………………………………………………………………… 40
CHAPTER 6: REGIONAL INJURIES ……………………………………………………………………. 44
6.1. Classification of the regional injuries …………………………………………………………….. 44
6.2. Head injuries ………………………………………………………………………………………………. 45
6.3. Spinal injuries …………………………………………………………………………………………….. 55
6.4. Chest injuries ……………………………………………………………………………………………… 56
6.5. Abdominal injuries ……………………………………………………………………………………… 61
6.6. Injuries to the pelvis and pelvic organs ………………………………………………………….. 61
6.7. Fractures of the face ……………………………………………………………………………………. 62
6.8. Fractures of the bones of the extremities ………………………………………………………… 62
CHAPTER 7: FALLS FROM HEIGHT ………………………………………………………………….. 65
7.1. General aspects …………………………………………………………………………………………… 65
7.2. Falls from standing position …………………………………………………………………………. 65
7.3. Falls from heights ……………………………………………………………………………………….. 66
7.4. Forensic issues in falls …………………………………………………………………………………. 67
3
CHAPTER 8: TRANSPORTATION INJURIES ………………………………………………………. 68
8.1. Road traffic accidents ………………………………………………………………………………….. 68
8.1.2. Injuries of the vehicles occupants ……………………………………………………………. 68
8.1.4. Injuries to motorcyclists ………………………………………………………………………… 73
8.1.5. Causes of death in road traffic accidents ………………………………………………….. 73
8.2. Train accidents ……………………………………………………………………………………………. 74
8.2.1. Lesions of the passengers in train crushes ………………………………………………… 74
8.2.2. Lesions of the pedestrians hit by the train ………………………………………………… 74
8.2.3. Lesions of passengers falling from the train ……………………………………………… 75
8.3. Plain accidents ……………………………………………………………………………………………. 75
CHAPTER 9: MECHANICAL ASPHYXIA ……………………………………………………………. 77
9.1. General aspects. Definition. Classifications ……………………………………………………. 77
9.2. Autopsy features …………………………………………………………………………………………. 78
9.2.1. General signs: ………………………………………………………………………………………. 78
9.2.2. Specific signs ……………………………………………………………………………………….. 79
9.3. Types of violent death ………………………………………………………………………………… 79
9.3.1. Hanging ………………………………………………………………………………………………. 79
9.3.2. Strangulation ………………………………………………………………………………………… 81
9.3.3. Suffocation ………………………………………………………………………………………….. 82
9.3.4. Thoraco-abdominal compression (“traumatic asphyxia”) …………………………… 84
9.3.5. Drowning …………………………………………………………………………………………….. 85
9.4. Laboratory examinations ……………………………………………………………………………… 87
9.5. From juridical point of view …………………………………………………………………………. 87
9.5.1. Accident ………………………………………………………………………………………………. 87
9.5.2. Suicide: ……………………………………………………………………………………………….. 88
9.5.3. Crime: …………………………………………………………………………………………………. 88
CHAPTER 10: DEATH CAUSED BY ENVIRONMENTAL FACTORS …………………… 89
10.1. General aspects …………………………………………………………………………………………. 89
10.2. Thermal injuries ………………………………………………………………………………………… 89
10.2.1. Low temperatures injuries ………………………………………………………………… 89
10.2.2. High temperatures injuries ……………………………………………………………….. 94
10.2.3. Injuries due to scalding …………………………………………………………………….. 98
10.3. Electrical fatalities …………………………………………………………………………………….. 98
CHAPTER 11: THE DEATH DUE TO CHEMICAL AGENTS – INTOXICATIONS … 103
11.1. General aspects ……………………………………………………………………………………….. 103
11.2. Types of intoxications ……………………………………………………………………………… 104
11.2.1. The Ethyl Alcohol Intoxication …………………………………………………………… 104
11.2.2. The Alcohol Intoxication (Other Than Ethanol) ……………………………………. 107
11.2.3. Carbon Monoxide Intoxication ……………………………………………………………. 109
11.2.4. Cyanide Intoxication …………………………………………………………………………. 112
11.2.5. Corrosive Acids And Alkalis Intoxication ……………………………………………. 114
11.2.6. Barbiturate Intoxication ……………………………………………………………………… 116
11.2.7. Benzodiazepines ……………………………………………………………………………….. 117
11.2.8. Pesticides Intoxications ……………………………………………………………………… 119
11.2.9. Parathion Intoxication ……………………………………………………………………….. 120
11.2.10. Narcotics/Opioids ……………………………………………………………………………. 121
11.2.11. Stimulants ………………………………………………………………………………………. 125
11.2.12. Hallucinogenes ……………………………………………………………………………….. 127
11.3. Investigation Of Drug Abuse Death …………………………………………………………… 129
CHAPTER 12: FORENSIC PSYCHIATRY ………………………………………………………….. 134
4
12.1. General aspects: mental illness ………………………………………………………………….. 134
12.2. Medico-legal psychiatric examination………………………………………………………… 134
12.3. Types of abnormal mental condition ………………………………………………………….. 135
12.4. Effect of alcohol or drugs on judgment ………………………………………………………. 143
12.5. Diagnosis of insanity ……………………………………………………………………………….. 144
CHAPTER 13: KILLING OR INJURY OF NEWBORN COMMITTED BY MOTHER
…………………………………………………………………………………………………………………………. 146
13.1. Definition. Legislation ……………………………………………………………………………… 146
13.2. Medico-legal examination of the newborn’s cadaver……………………………………. 147
13.3. Methods of killing the newborn by his mother…………………………………………….. 160
13.4. Medico-legal expertise in cases presumed to be killing newborn by his mother. 163
13.5. Examination of the place of delivery ………………………………………………………….. 165
CHAPTER 14: SEXUAL OFFENCES ………………………………………………………………….. 166
14.1. Classification: …………………………………………………………………………………………. 166
14.2. Natural offences ………………………………………………………………………………………. 166
14.2.1. Rape ………………………………………………………………………………………………… 166
14.2.2. Incest ……………………………………………………………………………………………….. 173
14.3. Unnatural offences …………………………………………………………………………………… 173
14.4. Sexual perversions …………………………………………………………………………………… 176
CHAPTER 15: DNA GENETIC FINGERPRINT …………………………………………………… 180
AND IT S IMPORTANCE IN MEDICO-LEGAL PRACTICE ………………………………… 180
15.1. Theoretical appreciations ………………………………………………………………………….. 180
15.2. DNA Profile – scientific and technological advances. …………………………………… 182
15.3. Advantages and disadvantages genetic fingerprinting method ………………………. 183
15.4. Scope of genetic methods …………………………………………………………………………. 184
15.5. Value and limits of DNA profiling as evidence in court ……………………………….. 185
15.6. Collection and preservation of biological samples for DNA determination …….. 186
15.7. Harvesting, transportation and storage of evidence………………………………………. 187
15.8. Peculiarities of identifying, harvesting, packaging and preserving biol ogical traces
or micro-traces present at the scene for crimes of murder and their possibili ties for
recovery by the method of genetic analysis…………………………………………………………. 191
15.9. Types of biological samples necessary for recognition of corpses with unknown
identity based on genetic molecule …………………………………………………………………….. 195
CHAPTER 16: GENETICS AND SEROLOGICAL LEGAL MEDICINE ………………… 196
16.1. Forensic genetics. DNA profile. ………………………………………………………………… 196
16.2. Expertise parentage. Forensic serology. ……………………………………………………… 196
References …………………………………………………………………………………………………………. 212
5
CHAPTER 1: INTRODUCTION TO FORENSIC MEDICINE
1.1. General aspect. Definition. History.
1.1.1. Definition of Legal Medicine
Legal medicine is the medical science that puts its knowledge in the service of
justice, in order to clarify causes that require certain medica l and biological specifications.
To this end, it had different names during the years: judicial medicine, law medi cine, etc.
The object of study of legal medicine resides in studying dea th (thanatology), the
causes leading to death (thanatogenesis) related to crimes against life on the one hand, and
in studying of the causes and the consequences of crimes against body integrity and health
of living persons on the other, as well as in researching certain biol ogical samples or
tissues isolated for identification during laboratory analysis.
1.1.2. Short History
Legal medicine is a science with deep traditions. One of the oldes t proofs attesting
cooperation between doctors and justice can be found in Hamurabi’s Codex ( 1792 – 1750
BC). Proofs can be also found in the biblical books of the ancient Hebrews and the
Egyptians, but it cannot be said that the ancient peoples had a real system of notions
regarding justice aspects. Significant achievements were ac complished in ancient Greece,
through its distinguished representative Hippocrates, who was interes ted in medical ethic
issues. There it has been established that medical science could e volve only through
practice (autopsy).
In the 16-th century was written the first legal medicine sc ientific treatise
(Ambroise Pare), which addressed issues such as lethal wounds, asphy xiation sudden
deaths and intoxications. In the 20-th century legal medicine was to be enriched with new
research fields regarding human heredity and serology.
In Romania, the first elements of legal medicine appeared around 1600, a nd further
important contributions were made by Mina Minovici, who wrote the fir st treatise of legal
medicine, and in his honor The Institute of Legal Medicine of Buchares t was named after
him.
6
1.2. Medico Legal Thanatology
1.2.1. Definition
Thanatology (Thanatos = the god of Death in Greek mythology) is the science that
studies the phenomena and the issues regarding death of the human organism.
Its purpose consists in establishing the kind of death (violent or nonviol ent), the
cause of death (the thanatogenerator cause), the thanatogenetic mec hanism
(thanatogenesys), as well as the time of death.
Death is the permanent and irreversible ending of life by disc ontinuing the vital
functions. It is generally a slow, progressive and gradual phenomenon. It is only in the
case of injury of the bulbar and mezencephalic centers that we can speak of death as an
instantaneous process.
1.2.2. The Medico Legal Autopsy and Postmortem changes
Between life and death there is an intermediary state called agony (Greek agon =
struggle, fight). Agony is the phase that precedes death, during which a struggle is fought
between life and death. It can last for minutes, hours, days or it m ay not occur at all in case
of some violent death. Unlike coma, which is reversible, agony is i rreversible. During
agony, consciousness (awareness) can be maintained (unlike in the case of coma).
From a clinical point of view agony is characterized by: superf icial, irregular
breathing, with Cheyne – Stokes or Kussmaul forms of dispnea: blood press ure drops to
zero.
1.2.2.1. Phases of agony
Agony goes through several phases:
• euphoric phase;
• diminishing of the relation functions (fixed look, hyppocratic face, slowed
down hearth beats, cyanosis, superficial, irregular breathing)
• complete immobility accompanied by body temperature drop and progress ive
suppression of all senses.
According to the consciousness level agony can assume three possible forms:
• delirious – in injuries of the CNS (Central Nervous System), ence phalitis,
intoxication, alcoholism.
• lucid – without seriously affecting the consciousness level
• alternant.
7
The agonizing are considered irresponsible for the crimes they may commit, and in
what concerns legal documents (donations, wills), these have legal value only when the
expert can attest scientifically that in the very moment of their writing that person was full
exercise of their judgment. Following the agony phase there comes death, explained by
serious dysfunctions of the gaseous metabolism that is anoxia.
The human tissues have different sensitivity to anoxia. Thus, the nervous tissue is
the most sensitive, resisting a maximum of 5 minute to anoxia, the marrow tissue 30
minutes, intestinal muscles 1 – 2 hours, etc
1.2.2.2. Phases of death
The death process has two phases:
• clinical death;
• biological death.
A. Clinical death
Clinical death lasting for about 5 – 6 minutes after breathing and blood circulati on
stop, up to the permanent state of death installing as a result of t he physical and
chemical altering of the nervous cell. During this period the res uscitation operation are
crucial.
Ceasing of blood circulation and breathing are signs of clinical dea th, while the
absence of corneal, pupilar reflexes, accompanied by mydriasys, th e absence of EEG
waves are signs of permanent (biological) death.
In this phase of death, organ transplant issues can be addressed. Thes e procedure can
be commenced only after installation of cerebral death, medically confirm ed by:
• clinical examination – profound non-reactive coma; absence of cerebr al trunk
reflexes (photo-motor and corneal).
• absence of spontaneous breathing confirmed by the apnea test.
• two EEG lines at six hour interval which attest the absence of c erebral electric
activity.
B. Biological death
Biological death is characterized by the cease of all vegetative functions wi th signs of
real death. The exact moment of real death is rather difficult to establis h.
The death diagnosis is established through a series of signs of de ath, as well as
cadaverous alterations classified as following:
8
Negative life signs (with indicative value only):
• position and general aspect of the body;
• cease of breathing and blood circulation;
• abolition of reflectivity;
• absence of cerebral activity (absence of corneal and pain response reflex es);
• dropped mandible, relaxed musculature, ajar eyelids, ocular modifications.
Actual death signs:
a. early cadaverous alterations (the cooling of the corpse, cadaverous lividities,
cadaverous rigidity, dehydration)
b. late cadaverous alterations (destructive, conservatory and artificia l)
a. Early cadaverous alterations
• a1. Corpse temperature loss is a consequence of the cease of blood circulation
and metabolism, followed by loss of heat to the environment. It star ts from the
surface of the body, continuing inward and depends on the temperature of the
environment. It was established that this usually progresses with 1 g rad Celsius per
hour at an environmental temperature of 15 – 20 grade Celsius, thus in 24 h ours the
temperature of the corpse becomes the same with the temperature of the
environment, or even lower. It is assumed that real death has insta lled when the
rectal temperature reaches 20 grade Celsius.
Medical legal importance :
– it is a sign of real death (biological);
– it serves to establishing the time of death.
• a2. Cadaverous lividities is determined by the cease of blood circulation and
accumulation of blood in the blood vessels of the declivitous areas of the bod y, as a
result of gravity, followed by hemolysis, diffusion and inhibition of tis sues. The
violet color determined by a low level of hemoglobin and progresses in three
stages:
hypostasis – installs two hours after death, and lasts jor up to 12 – 18 hours.
It can be initially noticed in the declivitous regions of the corps e in the form
of non-confluent bluish spots that subsequently join, appearing on the sides
of the neck and trunk. They disappear under finger pressure and appear
again when pressure is ceased. Changing the position of the corpse in this
9
stage lead to disappearing of the cadaverous lividities form the initial zones
and their reappearing in the new declivitous regions.
diffusion occurs 12 – 15 hours after death and lasts up to 24 hours. The
lividities diminish at digital pressure, but do not disappear complete ly; they
do not disappear when modifying the initial position of the corpse, but t hey
also appear in the new declivitous position. This happens because the blood
hemolyses and the colored plasma leaves the vessels and soaks the
neighboring tissues.
Imbibition installs 24 hour after death when blood hemolysis is complete
and putrefaction changes commence. During this stage, the lividitie s are
modified neither by finger pressure, nor by changing the position of the
corpse.
The cadaverous lividities must be distinguished from ecchymosis whi ch is vital
injuries. This can be done by sectioning the skin in the suspected ar ea, followed by
washing it with water. The cadaverous lividities are washed awa y, the tissues remaining
clear, while in the case of ecchymosis the blood spilled through te aring of the blood vessel
and coagulated in the tissues cannot be washed down.
The cadaverous lividities may be absent in some declivitous regions as result of
being compressed by the support on which the corpse lice, or by the clot hes ore in cases of
severe anemia. They can have specific placement: for example in the case of complete
hanging, in vertical position, they can be noticed on the interior limbs.
Medical legal importance:
– represents the certain and early sign of real death
– offers clues in establishing the time of death
– provides information regarding the position of the corpse and further alteri ng of
the position
– has orientate diagnosis value (for example the color pink-carmine in the case of
CO poisoning, because of carboxihemoglobin which gives the blood its color;
intense-red in the case of frozen corpses; brown in cases of i ntoxications with
methemoglobin substances.
• a3. Cadaverous rigidity: is the stiffening of the muscles after death, due by the
disappearance of the ATP from the muscles. The evolution of cadaverous rigidity:
it is first present, 3-6 hour after death in the jaw joint and it goes down to the
muscles of the neck, upper limbs, trunk, lower limbs and it reaches its maximum in
10
24 hours after death. The duration of full cadaverous rigidity may be between 24-
36 hours until it begins to fade in roughly the same order of muscle g roups as it
appeared. The usual method of testing cadaverous rigidity is by att empting to flex
or extend the joints.
Medical legal importance of cadaverous rigidity:
– is a sign of the real death;
– helps us to estimate: – the post-mortem interval;
– the position of the body after the death;
– the cause of death(ex: in stricnine poisoning a rigor mortis
is powerfully).
• a4. Deshidratation: The death body loses water, that’s why the skin takes a brown
color and becomes hard. This phenomenon begins with the thin skin (eyeli d, lips,
fingers, scrotum) and the cornea (with an aspect of opacification).
• a5. Autolysis : is a process ranging from autolysis of individual cells by i nternal
breakdown, to tissues autolysis from liberated enzymes. This process appears first,
in few hours after death, in the organs with a lot of enzymes (ex pancreas).
b. Late cadaverous alterations
b.1. Destructive processes – putrefaction (post-mortem decomposition)
It is a process induced by bacteria coming from the natural ca vities of the body
(intestine especially) and from environment. In an average temper ature climate, the
putrefaction begins at about 2-3 days in the unrefrigerated corpse. Th e first external
sign of putrefaction is fading of the lower abdominal wall, most ofte n in the right iliac
fossa where the bacteria laden caecum lies fairly superfici ally. This fading spreads
progressively over the abdomen which, in the later phase, begins to bec ome distended
by gas. After several weeks, the color of the skin may deepen to a dark green or almost
black.
The rate of decomposition is slower at the immersed corpses, mainly because of the
lower ambient temperature, the small oxygen concentration and protec tion from insect
and small mammal predators. For the putrefaction to appear is nece ssary the presence
of the oxygen.
b.2. Conservatory and artificial processes :
These processes stop the putrefaction, each of them by a different mechanis m.
11
Mummification: is a very rapid dehydration which appears in a warm
climate, with good ventilation (a body berried in the sand, at high te mperature,
for example).
Lignification : appears to the bodies which stay in a land with a great
concentration in carbon. The skin becomes brown and hard, the features of the
body and the injuries are well conserved.
Formation of the soaps that cover the body : to the corpses which stay in
water after the death. In water the skin is destroyed, and the fa t tissue forms,
with the salts from the water, yellow-grey soaps that cover the body and the
putrefaction is stopped.
Refrigeration : is the best conservatory method. By this method the body can
be conserved for thousand of years. It is so an artificial methods.
1.3. Medico-legal Cases
Forensic autopsy is mandatory in most jurisdiction in the following situation:
• Homicides
• Suicides;
• Accidents that occur on the job;
• Drivers in single car accidents;
• Sudden and unexpected death to children;
• Death of pilots in aircraft crashes;
• Natural death that might impact the community
• Fire deaths
• Accidental deaths caused by the negligence or reckless behavior of others
• Death of person in custody of the state or other agency
• Accidents that occur without a witness
• Accidents in which natural disease is a factor
• Sudden, unexpected deaths of apparently healthy persons
• Deaths in which the manner of death is not readily apparent
• Death in which litigation is reasonably expected
• Hospital deaths in which the quality of care is an issue
• Death in within 24 hours of admission to a hospital
• Suspicious deaths.
12
Autopsy is elective when:
• The client s legal representative or family want an autopsy performed.
• The on-duty physician believes valuable information pertaining to medic al care
may be obtained.
• There is a need for clarification of the circumstances of the death.
1.4. Forensic exam on cadaver and Forensic Autopsy
Objectives of the cadaver forensic exam :
1. Identification of the cadaver.
2. Establishing type of death (violent, non-violent, and inhibitory).
3. Establishing of the medical cause of death.
4. Establishing of the date of death.
5. Cause of body lesions, mode of production, conditions in which were produced.
6. Establishing, eventually, of one report of causal connections between the traumatic
lesions present on the body and cause of death.
For establishing of objectives mentioned above is obligatory to do:
1. Exam at the place of event.
2. External and internal examination on cadaver (forensic autopsy).
3. Examination of the eventually involved crime tools.
4. Examination of the aggressor.
Exam at the place of event :
• Is done together with the Police Authorities and Public Prosecutor’ s
Department Authorities.
• Is written a Finding Minute (Verbal process) at the place of the event in
which are recorded:
o position of cadaver;
o lesions and traces found on the body or on its clothes;
• There are not expressed any appreciation about the cause of death unle ss after
the complete autopsy of cadaver which is obligatory.
Forensic autopsy :
• starts with external exam of cadaver
• Cadaver identity:
13
o in case of known identity persons are recorded: approximate age, sex,
height, constitution;
o in case on unknown identity persons is done a detailed description of
the face (spoken portrait) – is described the hair, its color, length, color
of the eyes, shape of the nose, shape of the mouth – as well as a
detailed description of the exterior aspect of the cadaver, insist ing on
some particularization signs (scars, pigmentations, anomalies, tat toos).
Also is done a detailed description of dentition (caries, missing teeth,
dentist works).
o For these persons is necessary to take finger prints and to take s ome
judiciary photos.
• Signs of real death:
o Early cadaverous signs: Cooling of the body, Dehydration Cadaverous
lividities, Cadaverous rigidity
o Late cadaverous signs: Putrefaction, Mummification, Lignification
• Signs of violence:
o Eventually present are recorded starting with cranial extrem ity
downward ventral and dorsal.
o Are described: the localization, shape orientation and angle,
dimensions, any present changes around them.
o In case of traumatic lesions with no continuity of tegument are
sectioned but without changing the morphologic character of it.
o For penetrating wounds is sectioned the tissues in layers for def ining
the direction, trajectory, and dimensions.
By the detailed description of the traumatic lesions sometimes is
necessary to take some pictures or to draw.
• Other signs: eventual local (any inflammatory processes, skin disease,
circulation diseases) or general diseases(edema, icterus, etc), specifically their
signs;
• Signs of treatments: injections, surgical operations.
14
1.5. Forensic exam report
This report includes three parts:
1. Introductive part
2. Descriptive part
3. Synthesis part
1.5.1. Introductive part:
Introductive part includes three sub parts:
• Preamble
• History of events
• Preliminary exam
Preamble includes:
• name, surname and doctor’s specialty who’s doing the autopsy;
• act in base of which is done the autopsy (ordinance, address) with
specification of number, emission date and unity which emitted it ( police,
public prosecutor’s department);
• data about the cadaver id:
o In case of known cadaver id – is noted the name, age, sex and home
address – data which are from the identity card,
o In case of unknown cadaver id – is noted sex, probable age (with 10
years difference) and place where it was found deceased.
• date of death;
• date and place where the autopsy is done.
History of events : is recorded in chronological way all the events connected to the
actual case. Sources of information are: minutes (including declar ations of relatives
and background) and medical documents (file, exit bulletin from the hospi tal,
health card, etc). There are three situations of history:
• Case in which there is no data about the case, is recorded from mi nutes,
place, date and background of the death;
• Case of sudden deaths or rapid violent deaths, history is short including t he
symptoms heading the death, date or hour of installing of symptoms and
date or hour of death or place, date and type of the accident;
• Case of hospitalization of the victim in the hospital is extracte d from file:
date and hour of hospitalization, date and hour of decease, hospitalization
15
diagnosis, treatment, evolution, complications, and symptoms before the
death.
• Data from the history are not obligatory to coincide with the concl usions of
forensic examination, is just the probable information.
Preliminary examination is requested just in some situations, like:
• case of electrocution, when together with an expert is investiga ted the state
of electric devices;
• Case of homicide, when is examined aspect of clothes, shoes of the victim.
1.5.2. Descriptive part includes two sub parts:
External cadaver examination.
Internal cadaver examination
In both sub parts are described the aspect of the lesions and of interna l organs. There
are not used notions of diagnosis.
1.5.3. Synthesis part which includes:
Anatomic-pathologic diagnosis : is a line of diagnostics based on the description
in the descriptive part;
Complementary examinations:
• Histopathological exam;
• Toxicological exam (blood alcohol level, alcoholuria, toxicology);
• Serological exam (vaginal secretions in homicide followed by murder);
Conclusions of the forensic exam report which includes:
• type of death (violent, non-violent);
• medical cause of death (e.g.: acute myocardial infarction);
• mechanism of death, of body lesions and causal connection between lesi ons
and decease;
• date of death;
• blood alcohol level.
16
CHAPTER 2: SUDDEN DEATH
2.1. Definitions
• The sudden death is that which occurs suddenly, unexpected, to an apparently
healthy person, or to a person suffering from a disease without le thal potential; it is
a death clinically unexplained or otherwise obscure, even though there need to be
no unnatural element in their causation.
• World Health Organization defines sudden death as “death that is unknown or
sudden and occurring within 24 hours from onset of symptoms” (Knight B., 1996).
• Sudden death is” unexpected death following so rapidly from the onset of
symptoms that the cause of death could not be certificated with conf idence by a
medical practitioner familiar with the patient”
• The description “sudden”, “unexpected”, “unexplained”, is the reason for medico-
legal investigation.
2.2. Sudden death in adult age
In adult age, the causes of sudden death are, in order of the frequency:
1. Cardiac diseases.
2. Respiratory diseases.
3. C.N.S. diseases.
4. Gastrointestinal and genitor-urinary diseases.
2.2.1. Sudden death from cardiac diseases
In adult age, ischemic heart disease is the most common cause of sudden death.
Predisposing factors:
• Alcohol abuse
• The acute stress
• Plentiful meals
• Sexual effort
• Atmospherical conditions
• A hard work
17
2.2.1.1. Coronary atherosclerosis
Is the most frequent cause of sudden death in adult age. The mechanis m is the stenosis
or the occlusion of one or more major branches of coronary arteries by atheromatous
lesions, or one of the complications of such lesions. Most of the cardi ac pathologists claim
that at least 80% of the normal lumen must be lost before myocardi al necrosis occurs.
Almost all myocardial infarcts are caused by atheromatous lesions and the ir complications.
The autopsy diagnosis of myocardial infarction :
The following appearances are typical of the stages of myocardial infarcti on:
• for the first 8-12 hours, no definite naked-eye changes are visible. Thus, any person
dying in the first few hours after a complete coronary occlus ion, will show no signs
of infarction at post-mortem examination.
• at the end of this period, the first sign is oedema of affected ar ea of muscles, which
cause palor of it. The cut surface becomes more granular and dull when cut by a
sharp knife.
• from about the end of first day, progressively through the second and thi rd, the area
becomes better demarcated and yellow, with red streaks –“tigroid aspect”.
• after a few days, the infracted area becomes softer and mor e friable (myomalacia
cordis). In this stage, ruptures of the heart wall may occur into the pericardial sac;
• from the third week and later, the center of the infarct becomes gelatinous, with a
translucent grey colour;
• during the next month or two, depending on the size of the infarct, fibrosi s replaces
the dead muscle to from a scar.
Complications of myocardial infarction:
• rupture of the heart with haemopericardium and fatal cardiac tamponade;
• mural thrombosis-in infarcts involving the endocardium;
• pericarditis – in full thickness infarcts;
• myocardial fibrosis;
• cardiac aneurysms;
Causes of death in myocardial infarction:
• deficiency in the pomping action of the ventricles;
• ventricular fibrillation
• cardiac arrest;
18
Number of sudden death from coronary insufficiency does not have myoca rdial
infarction. In these cases, death occurs from a rhythmical defe ct due to the vulnerability of
myocardium and especially the pacemaking and conducting system at ischemia and
hypoxia. In this situation, disturbances of the rhythm, from ectopic bea ts to atrial
fibrillation or to ventricular fibrillation and cardiac arrest may occur.
2.2.1.2. Hypertensive heart disease:
An extremely common finding at autopsy is of left ventricular hy pertrophy with no
other evident cause of death. A patient with hypertensive cardiac hypertrophy is always a
candidate for sudden death, either from the direct effect on the m yocardium or from a
cerebro-vascular accident.
2.2.1.3. Valvular diseases:
Aortic valve disease with calcific aortic stenosis,
• Appears usually at men over 60 years old.
• Sudden death is common in these cases, partly because of the low pr essure in the
aortic sinuses and coronary ostia and also because of the relative coronary
insufficiency caused by the massive increase in the muscle mas s of the
hypertrophied left ventricle.
Endocarditis: this is caused by bacterial proliferation on the mitral and aor tic valves,
frequently at the intravenous drug user.
Floppy mitral valve syndrome
– mechanism of death is ventricular arythmia.
2.2.1.4. Cardiomyopathies:
It is a myocardial dysfunction characterized by a large he art, absence of hypertension and
valve lesions. From morpho- etiological point of view, we have three forms:
• Congestive cardiomyopathy (ex. alcoholic myopathy) – the heart is globular due t he
hypertrophy of the wall and dilatation of the lumen of the heart. The cause of death
is a congestive cardiac failure.
• Hypertrophic obstructive cardiomyopathy.
• Obliterative cardiomyopathy.
2.2.1.5. Rupture of an anevrysm:
Is the most frequent extra cardiac cause of sudden death arising in the cardio-
vascular system.
19
There are three types of aortic aneurysms, all capable of catastrophic ruptur e:
• the atheromatous aneurysm, mainly in the abdominal segment of aorta.
• rupture of a dissecting aneurysm of the aorta, where the basic l esion is a
degeneration of the aortic media. It is the second most frequent ca use of
hemopericardium and cardiac tamponade.
• syphilitic aneurysms are now uncommon.
Fatal aneurysms of other vessels than aorta are rare apart from cere bral arteries
2.2.1.6. Acute coronary artery dissection
In this case we have: absence of atherosclerosis, spontaneous or du e to trauma, limited to
coronary artery, caused by the extension of an aortic dissection into coronary artery.
2.2.1.7. Congenital anomalies of the coronary arteries
• single coronary artery;
• coronary artery hypoplasia;
• left main artery arising from the right sinus Valsalva.
2.2.1.8. Pericarditis
2.2.1.9. Myocarditis:
It is usually found in young adults who have died suddenly and unexpectedly.
Histologically, we find minute foci of inflammatory cells in the myocardium and this has
been taken to indicate some viral myocarditis. We can consider that this is an infl ammation
of the myocardium caused by: infectious, toxic, inflammatory agent s or connective tissue
disorders.
2.2.2. Sudden death caused by respiratory system disorders
2.2.2.1. Pulmonary trombembolism
• Is an extremely common cause of sudden death, more frequent in women. It is
more common with advancing age, with obese subject. In the majority of cases
there is a predisposing factor such as trauma, surgical operat ion, confinement to
bed or immobility from another cause. Death is rapid, accomplished by intense
cyanosis and breathlessness. If the embolism is on a small pulmona ry vessel and if
the person survives a sufficient period of time, pulmonary infarction ma y occur.
Rarely the trunk of the pulmonary artery is affected; more ofte n are interested
smaller vessels. Experimentaly it was proven that the cease of maximum 75% from
the pulmonary circulation is not followed by death.
20
• Macroscopically pulmonary infarct is usually peripherally locat ed, dark red brown
and wedge shaped.
2.2.2.2. Respiratory obstruction, due to:
• rupture of retropharingeal abscess;
• diphteria, with laryngeal obstruction;
• fulminating epiglotitis caused by Haemophilus influenzae;
• laryngeal papiloma.
2.2.2.3. Bronchial asthma: The mechanism of producing death is still obscure.
2.2.2.4. Pneumonia: especially fulminating viral pneumonia, or bronchopneumonia.
2.2.2.5. Pulmonary tuberculosis: by rupture of a blood vessel in a cavity.
2.2.2.6. Acute epiglotitis: fulminating epiglotitis caused by haemophilus influenze in
children represent a major pediatric emergency. To save live may require rapid intubation
or tracheostomy.
2.2.2.7. Hemoptysis:
• it is caused by: pulmonary tuberculosis, bronchial tumors, lung abscess;
• cause of death: exsanguinations when aorta is eroded; smaller bleeds may fill the
air- passages and cause asphyxia-type death and sudden flooding of t he larynx
cause vagal inhibition – type death
2.2.3. Sudden death caused by central nervous system disorders
2.2.3.1. Rupture of cerebral aneurysm
The cerebral aneurysms may be congenital or formed during life , caused by
inflammatory vascular diseases. The most frequent localization of the cerebral aneurysms
is: circle of Willis and internal carotidis.
Spontaneous rupture of an aneurysm in the circle of Willis at the bas e of the brain,
is one of the most common cause of death in young to middle-aged adults, i f coronary
diseas is excluded.
At the autopsy we may find subarachnoid haemorrhage, but the most dense
haemorrhage will be over the base of the brain, because the usual poi nt of bleeding is in
the circle of Willis. The blood can spreads laterally covering , sometimes, the whole
surface of the cerebral hemispheres, the hind brain and down into the spinal canal.
2.2.3.2. Cerebral tumor: Cerebral tumor from a mute cerebral zone, without any
symptoms, may cause an intracerebral hemorrhage or a big cereb ral edema, followed by
sudden death.
21
2.2.3.3. Intracerebral hemorrhage: preceded by a previous strokee or history of
hypertension, is a frequent cause of rapid and unexpected death.
2.2.3.4. Non traumatic subarachnoid hemorrhage: are caused by rupture of a saccular
aneurysm at the base of the skull (85% of cases), nonaneurysmal lesi ons (10% of cases)
and rare vertebral artery dissection, cavernoma, etc.
2.2.3.5. Meningitis and meningoencephalitis: these diseases are caused by
Pneumococcus, Menigococcus, Listeria, Haemophilus Influenzae.
2.2.3.6. Cerebral Infarction
• causes: embolism (70% of cases) and thrombosis (aprox. 25% of cases).
2.2.3.7. Sudden death in epilepsy : It may occur in prolonged status epilepticus but also
without being in status epilepticus. The mechanism of death is obscur e. Epilepsy may be
an acceptable cause of death only after a negative autopsy and w hen all the investigation
has been completed.
2.2.3.8. Hydrocephalus: cause of death is sudden increase in intracranial pressure.
2.2.4. Sudden death caused by digestive system disorders
2.2.4.1. Gastrointestinal bleeding due to:
• gastric or duodenal peptic ulcers
• carcinoma of the stomach(may perforate a major vassels)
• esophageal varices.
• colonic lesions or hemorrhagic diatheses : carcinomas/ ulcerative colitis.
• rupture of abdominal organs: ex. Spleen.
• rupture of an ectopic pregnancy.
2.2.4.2. Mesenteric thrombosis and infarction of the intestine
2.2.4.3. Strangulated intestine / strangulated hernias (femoral or inguinal)
2.2.4.4. Fulminating peritonitis due to:
• acute appendicitis and appendix abscess
• perforation of the colon with carcinoma, diverticulitis
• a perforated peptic ulcer leads to a chemical peritonitis
2.2.4.5. Hemorrhagical acute pancreatitis: causing electrolyte abnormalities
2.2.4.6. Hepatic disorders due to:
• fatty liver: death is caused by metabolic and electrolytic imbalance
• alcoholic cirrhosis: death is caused by hepatic failure, metabolic disorder
and electrolytic imbalance.
22
2.2.5. Sudden death from the genitor – urinary system
2.2.5.1. Ectopic pregnancy: usually in the tubes, can rupture with massive intraperitoneal
hemorrhage.
2.2.5.2. Induced abortion: may produce: bleeding, air embolism, perforation of vagina or
uterus, infection and acute intoxication by using toxic substances
2.2.5.3. Amniotic embolism: causes death of the women immediately after the birth.
2.3. Sudden infant death syndrome (SIDS)
One of the major causes of unexpected, postneonatal infant death;
SIDS is a term used when infants (under one year of age) die suddenl y and
unexpectedly during sleep and the cause remains unknown; clinicopathologic al profile
is characterized by recent antemortem good health, male gender, prone sleep position,
maternal smoke exposure, and higher death rates during winter months.
In the first year of life, the most common causes of sudden death a re the acute diseases
of respiratory system, like: viral pneumonia and bronchopneumonia.
In summer, on the first place is the acute dyspepsia which may cause death in less than
24 hours by massive dehydration.
Another causes of sudden death in children:
• allergy to cow milk;
• viral encephalitis;
• cardiac malformation;
• Rh incompatibility – due to the sudden death shortly after birth, and so on.
23
CHAPTER 3: EXAMINATION OF ALIVE PERSONS
3.1. General assessment
It is respect the Emergency Ordinance Nr 1/2000. Examination is done by the Forensic
Doctor in the next cases:
• Defining the sex, virginity, sexual capacity, age, appearance and ph ysical
development, physical identity, for establishing the paternity;
• Defining the presence of diseases, traumatic lesions, infirmity a nd work
capacity in connection with these situations;
• Defining the Obstetrical State.
These examinations may be requested by:
• The present person if it is 14 years of age;
• One of the parents in case of minors;
• Tutor or the Tutorial Authority for the persons under the Guard;
• Persons who are taking care of minors others than mentioned previously;
• Director of the Institution for persons living in an Institution (like: dome trey,
hospital, boarding school, etc.);
• Commander of the place of imprisonment for the prisoners or the Authori ty of
the Penal Pursuit for the restraint persons;
Examination of live persons is done by the Forensic Expert alone or i n some
compulsory cases by a Committee in which is one Forensic Expert and Doctors
specialized in the same field (e.g.: Psychiatric forensic ex amination, forensic
examination implying postponement or interruption of imprisonment, etc) . Forensic
Doctor is the President of the Committee.
Resulted conclusions after the examining of live persons are writt en down in a
Certificate (Act, paper) especially for this occasion, which may be:
Forensic Report of Examination : – is done at the request of Authorities of the Penal
Pursuit or of Judge Instances in the period of Penal Pursuit. It appea rs as an
attachment Certificate to another Certificate typed initiall y and is not in Emergency
State.
Forensic Finding : – is done at the request of Authorities of Penal Pursuit before
starting of the Penal Pursuit; is a Forensic Certificate of Emergency St ate.
24
Forensic certificate : – is delivered at the request of interested persons in all cases
mentioned above and more exactly:
• traumatic lesions or other body injuries (aggressions, car accident , accident
at the place of work, etc.).
• any infirmities and incapacities following the trauma.
• virginity, defloration, etc.
• sex, age, etc.
• psychical state just in the case of any Disposition Act (like: sale, donation,
will/testament, etc).
3.2. Forensic Certificate
Forensic certificates are used by Authorities of Penal Pursuit and Law /Judge Instances.
To deliver forensic certificates are levied/perceived taxes which are fixed by the Notice
of the Health Minister. Forensic Certificates are stamped with fiscal stamp.
3.2.1. Component parts of the forensic certificate:
3.2.1.1. Introduction
includes:
Preamble: with:
• data about the examiner.
• number of registration, number of the payment receipt.
• place and date of the examination (the time, if the examination is done
before 24 hours from the event).
• data about the examined person (compulsory from the identity card).
History of the events: includes type and date of the injury (ca r accident, accident at
the place of work, aggression, rape, etc). Is a part affirming t he declaration (is
following to prove that in conclusions).
3.2.1.2. Description
includes:
Description of the injuries.
Noting suffered symptoms (eventually).
Result of the complementary examinations which may be:
• anterior to the forensic examination
25
• requested by the Forensic Doctor when lesion’s picture or symptom s
require it
In the description of the lesions one has to mention:
• type of lesions: ecchymosis, hematoma, contusion, abrasions, fracture, disloc ations,
sprains, etc.
• position of the lesions: anatomical region or part of the body, is repor ted to the
basal bone;
• number of the lesions: when number of the lesions is big and are situat ed at very
small distances, is described on whole reporting to the anatomical region (e.g.: on
the back are found multiple ecchymosis with the diameter of 4/3 cm and 8/6 cm);
• color of the lesions (indicates the period );
• shape of the lesions, reproduces exactly the shape of the tool used;
• dimension of the lesions:
o for lesions without continuity, note length and width.
o for wounds: depth is appreciated by describing the anatomic plan which
forms the base of it, but it is not probed.
• the position of the big axe of lesions (transverse, longitudinal); in w ounds the
presence and the aspect of the angle and the aspect of the margins;
• the content of the wound (pieces of glass, soil, etc)
• some signs of the treatment (bandages, gypsum body, etc)
Correct description of the lesions allows making the:
3.2.1.3. Conclusions
include:
prove reality of the injury;
age of traumatic lesions;
mechanism of production of the lesions, direction of the hits/strikes, t ype of the
hitting object;
period of medical care;
Methods of forensic examination differ from the clinician doctor.
For the estimation of the body injuries severity for the penal int egration of the event a
basal criteria is period of medical care for healing .
26
This period of medical care means the period of time in which heal ing of the injuries is
needed application of a therapy and not to the time of anatomical heal ing and not to the
time of temporary incapacity to work (medical leave).
3.2.2. Juridical Estimation of the Event after the time of medical care:
• Until 10 days (car accident) or 20 days (aggression) – is considered contravention
(is paid a fee);
• Between 10-60 days (car accident) and 20-60 days (aggression) – is cons idered
offence (penal file); reconciliation between the parts removes the penal fi le;
• Over 60 days – penal file without the possibility of reconciliation be tween the
parts, even they do the penal file is considered.
27
CHAPTER 4: DEATH DUE TO MECHANICAL AGENTS – THE
PATHOLOGY OF WOUNDS
4.1. Definition and classification of injuries
4.1.1. Definition: a wound or injury is damage to any part of the body through the
application of violence.
4.1.2. Classification of injuries:
Mechanical Injuries
Produced by blunt weapon: ecchymosis (bruises), hematoma, abrasion,
laceration;
Produced by sharp weapon: incised wound, stab wound, chopping
wound;
Produced by firearms: gunshot wounds.
Physical Injuries
Thermal Injuries:
• Produced due to cold: local hypothermia, frost bite, trench
foot, immersion foot, general hypothermia;
• Produced by local application heat: burns, scalds;
• Produced by general application of heat: hyperpyrexia,
heat exhaustion, heat cramps.
Electricity: lightning.
X- Rays
Radioactive substances
Chemical Injuries
Corrosives – acids/ alkalis .
Irritants – weak acids and alkalis .
Biological Injuries
4.1.3. Another classification
Wounds in which the skin is intact: bruises, hematomas;
Wounds in which the skin is completely affected: abrasions, lacerations, wounds
(incised wounds – cuts or slashes and stab wounds; split wounds, prick wounds,
gunshot wounds).
28
4.2. Types of injuries
4.2.1. Abrasions (GRAZES/SCRATCHES)
Characteristics: An abrasion is the most superficial of injurie s; it does not penetrate the
full thickness of the epidermis. Thus, the pure abrasion does not bleed, as blood vessels
are confined to the dermis. Because of the corrugated nature of the dermal papillaea,
many abrasions enter in the corium and bleeding commonly occurs. If the person is
alive, in 12-24 hours a brown crust appears a white track which disap pears in time,
without scar.
When death ensues soon afterwards, the abrasions becomes stiff, leat hery, and a
pachement-like brown color as a result of the drying of the moist exposed surface (for
example in the ligature mark of hanging or strangulation).
For the abrasions we may describe:
The place-anatomic region;
topographical lesion;
a fixed guiding mark on the body;
the existence and the color of the crust;
the shape;
the size;
the direction.
Types of abrasions:
Tangential or brush abrasions;
Crushing abrasions;
Fingernail abrasions;
Postmortem abrasions.
Tangential or brush abrasions : Most abrasions are caused by a lateral rubbing action
rather than by vertical pressure. The direction of the tangenti al force can be determined
by tags of epidermis dragged to the terminal end of the abrasion.
Crushing abrasions : When the impact is vertical to the skin surface, the epidermis is
crushed and an imprint of the impacting object is stamped on the surfac e. The lesion is
slightly depressed below the surface unless an underlying bruise or local oedema
bulges the tissues. This abrasions are the ones that most clearl y reproduce the pattern
of the injuring object (for example the marks of a vehicle radiator on a pedestrian
victim).
29
Fingernail abrasions : May be linear scratches (if the fingers are dragged down the
skin(in sexual attacks, child abuse) and short straight or curved marks when the skin
is gripped in a static fashion (in strangling, on the neck we may s ee: one fingernail
abrasion on a side and four fingernail abrasions on the other side, wit h a bruise to the
base);
Postmortem abrasions: Postmortem abrasion is common.
• They may have a variety of causes, including: dragging a corpse or buffeting in
flowing water; insect bites, especially ants; damages at the autopsy. As the
postmortem interval increases, the skin becomes more fragile.
• Postmortem abrasions are: yellow, translucent, absolutely lacking of any color
change at the edge.
4.2.2. Bruises (Contusions)
Definition: a bruise is an extravascular collection of blood that l eaked from blood
vessels damaged by mechanical impact.
We must describe to a bruise:
• The place-the anatomic region, the topographical region and a fixed g uiding
mark on the body;
• The size;
• The color;
Factors affecting the size of the bruise:
The space outside the vessels for free blood to accumulate- this ex plains the
easiness with which bruising appears in lax tissues such as eye- socket or scrotum
and its rarity in the sole of the foot or palm of the hand, where ther e is a dense
fibrous tissue and restrictive fascial planes preventing the accumulation of b lood;
The size of the hemorrhage, depending on:
• the intensity of the injuring force;
• the size and density of the vascular network of the damaged region;
The presence of the bone under the skin ( head, chest, shins) favors the appearance
of the bruises;
The depth at which the bruise is placed (its profoundness).
The fragility of the blood vessels and the coagulability of the blood;
A bruise may appear at a different place from the point of impact, especiall y when
blood extravasates in the deep tissues. Also, bruises may move because of gravity.
30
Alteration of bruises in time:
• In the first hour, the bruise is red (HbO2).
• After a few hours ,the bruise is bluish (HbO2 passed into reduced Hb)
• In 3-5 days, the edges become green (biliverdin pigment).
• In 7-8 days, the whole bruise is yellow (due to hemosiderin pigment)
• After 10-20 days, the bruise disappears, depending on the size and depth of the
bruise.
Hematoma: This kind of injury appears when a big vessel is hurt and an important
quantity of blood is accumulated in the tissues. If the hematoma is s uperficial, the
covering skin is bruised. Frequently, hematoma needs a surgical treatment to evacuate
the blood. It may compress anatomical structures like nerves, vess els, muscles and so
on. The hematoma may be formed in the natural cavities of the body, l ike in
pericardium, in the abdomen, surrounding the kidneys or in organs, with severe
evolution
4.2.3. Lacerations
Definition: laceration is the type of injury consisting in penetra tion of the full thickness
of the skin.
The laceration is produced with a blunt object which crushes the tissue s. A pelicular
form of laceration appears in the regions where the skin is press ed between the bone
and the blunt object. The result is the crack wound (for example on the scalp).
The crack wound must be differentiated from the incised wound, having shar p
margins, identical with the incised wound (the difference is that the crack wound has
tissue strands across the interior of the wound).The skin surrounding a laceration may
have abrasions and bruises. The main complication of the laceration is the infection.
A laceration may be distinguished from an incised wound by :
• the bruising and the crushing of the margins;
• the persistence of tissue strand across the interior of the wound (f ascial bands,
vessels, nerves). In an incised wound, these are divided;
• if the area is covered with hair, as on the head, intact hairs will survive across the
wound; an incised wound divided them;
• the laceration has obtuse angles; the incised wound has acute ang les, with a little
abrasion to the end, due to the knife taking out of the wound.
31
4.2.4. Wounds
4.2.4.1. Incised wounds:
– are caused by a sharp object (a knife, a razor, a glass, and so on).
A. Cuts or slashed wounds:
Definition: when an incised wound is larger than deep, we talk about a “cut” or a
“slash”.
Such wounds may be produced by a knife, a razor, a razor-blade, a glass , and are
typical for a fight and also for defense wounds; The defense may be : passive (the
slashes appear on the dorsal part of the hands and forearms) and act ive (the slashes
appear on the palms and on the fore part of the forearms- the victim tries to catch the
weapon).
The slash may be deeper at the entry end and becomes progressively shallower as the
wound approaches the distal end, where a linear abrasion called “m ouse tail” will
appear.
Slashed wounds are less dangerous than stabs, as the relative shallowne ss of the wound
is less likely to affect vital organs-the arms and the face being the most common
targets.
Bleeding is the most serious complication of slashes, through it wi ll be external and
more accessible to immediate treatment than the hidden internal bleeding of a stab
wound.
B. Stab wounds:
Definition: a stab wound is an incised wound that is deeper than wider.
Stab wounds are extremely common in homicide. The stab wounds are very dangerous
because they may hurt a vital deep organ.
The characteristics of a stab wound are very important for the for ensic expert because
they offer datum on:
the dimensions of the weapon: the length of the incised wound on the skin is equal
to the maximum width of the knife and the depth of the wound in the tis sues is
equal to the minimal length of the knife (because in the moment of the impact, the
soft tissues are removing and the blade penetrates through a bigger l ength than its
blade length);
the type of blade: with a single or double cutting edge. If it is a blade with a double
cutting edge, both ends of the wound appear sharply cut, like a “V-point” a t the
32
extremities. If the blade has one cutting edge, the wound has a si ngle sharp end, the
other being larger. At the sharp end we may find the abrasion named “mouse tail”.
movement of the weapon in the wound-if the knife is twisted in the wound, the skin
defect will be enlarged. This twisting may occur either by th e knife being actively
moved in the wound by the assailant, by the body moving relative to the knife, or
by a combination of the two;
the direction of the stab wound is important in homicides. We use the a ppearances
of the skin wound and the track in the deep tissues.
4.2.4.2. Split wounds
Definition: the split wounds are produced with sharpening and heavy weapons like:
axe, hoe, and so on.
Split wounds are a combination between laceration and incised wound: the split wound
looks like an incised wound on the skin and like a laceration in the deep tissues,
because these are compressed and destroyed by the weight of the weapon. Frequently,
the bones are fractured and vital organs are damaged. That is why, that kind of wound
is very dangerous for life.
Split wounds are, usually, found in homicide and rarely in suicides and sometimes in
accidents (in this last case are situated on the hands or on the forearms).
4.2.4.3. Prick wounds
The weapons used in these cases are: needles, knitting needles, nails.
The weapon pushes the tissues laterally. On the skin, we will find a red point if the
diameter of the weapon is small (for example sharp needle) or a little wound w ith sharp
edges when the diameter of the weapon is bigger (for example nail).
This kind of wounds may cause death if the weapon penetrates the heart or the fontanel
(in infanticide cases).
33
CHAPTER 5: GUNSHOT WOUNDS
5.1. The mechanics of the missile injury
The missile injury is caused by the transfer of energy f rom the missile to the tissues.
For damage to occur, some or all of the kinetic energy of the missile has to be absorbed
by the target tissues. The amount of kinetic energy possessed by a projectile , accords to
the formula: MV/2, where M- the missile mass and V- velocity
The mode of injury depends on the velocity of the missile:
Relatively slow projectiles are those traveling at up to the speed of sound in
the air (340 m/sec), which includes all non-explosively missiles li ke cross low
bolts and air-rifle pellets, as well as most revolver bullets. These, mechanically
thrust aside the tissues along a track only slightly wider than t he missile. The
tissues are lacerated or crushed, secondary damage occurs from r upture of
blood vessels and other structures, and secondary and tertiary damage is caused
by displaced bone and cartilage fragments.
Above the speed of sound in air – a missile passing though tissue sends a
shock wave of compression ahead of the laceration track, this wave being
propagated at about the speed of sound in water (1500m/sec). Though this wave
lasts only for a brief period, it raises the tissue pressure to extreme values, up to
thousands of kilopascals. In tissues like brain, liver, muscle, this may cause
severe disruption within a wide zone around the bullet track, and may be
propagated down hollow fluid-containing vessels to cause distant vascula r
damage.
High velocity projectiles produce yet another phenomenon, that of cavitation.
The missile accelerates the molecules of the tissues adjacent to the tr ack, so that
they continue to move centrifugally outwards, even after the missil e has
traveled outwards. This forms a cavity around the track that is fa r wider than
the diameter of the projectile. Solid organs such as brain and liver are affected
more than spongy matrices like lung. Those tissues that contain m ost water are
most severely damaged by penetrating missiles and high-veloci ty missiles,
damage being proportional to the specific gravity of the tissue injured.
34
Velocity of the missile and the mode of injury:
Slow projectiles (340m/sec.) – thrust aside the tissues along the track only
slightly wider than the missile.
Above the speed of sound in the air – a shock wave of compression ahead of t he
laceration track.
High-velocity projectiles- the phenomenon of “cavitation”.
5.2. Types of weapon
The nature of firearm wounds varies considerably with the type of w eapon employed. In
context of wounding, guns are of two main types:
5.2.1. The smooth-bore weapon or ”shotgun”
A shotgun consists of one or more metal barrels of relatively wi de diameter, which are
smooth on the inner surface. A shotgun often has two barrels. They fire a variable
number of spherical lead shot (pellets), which emerge from the end ( muzzle) from
where they gradually diverge in a form of a long, narrow cone.
“Country guns” – In developing countries, in some rural and poor areas of ot her
countries, in subversion and terrorism, and sometimes in juvenile hands, wea pons and
ammunition may be “home – made”. This type of guns raises a lot of problems for the
pathologist, especially because irregular missiles are employed.
5.2.2. The rifled weapon
Handguns, rifles, air – rifles and military weapons differ from shotgun bec ause they fire
one projectile at a time, through a thicker barrel that has spira l grooves machined on its
inner surface, which gives it a rotating movement. This has a gyr oscopic effect that
increases the stability of the bullet’s trajectory and hence the accurac y.
5.3. Wounds
5.3.1. Wounds inflicted by a smooth-bore shotgun
When a shotgun is fired, a compact mass of shot emerges from the muz zle and then
begin to disperse, the divergence increasing progressively as the distance grows. A
short flame and hot gas follows the shot. High pressure and temperat ure exists just
outside the muzzle, but this rapidly expands and cools. This gas is c omposed of oxides
of nitrogen, carbon dioxide, hot air and other compounds, but the one of interest to the
pathologist is carbon monoxide.
Soot from the combustion of propellant is expelled, along with some flakes or gra ins of
propellant that may be still burning. The wads are also expelled, t heir nature depending
35
upon the type of cartridge. The appearance of the wound is greatly m odified by the
variation in range and it is convenient to describe them in terms of i ncreasing range of
discharge.
We describe 3 elements:
• Entry wound
• Exit wound
• The internal track
The direction of a shotgun injury: Where the discharge has been at right angles to
the body surface, the shape of the wound will be symmetrical and cir cular. In all other
position, an ellipse will be traced out, its elongation increasing as the angle between
them decreases. The track of the wound in the deep tissues may be established and this
line projected backwards to indicate the discharge direction relative to the body.
5.3.1.1. Entry wounds
a. Shotgun contact wound.
• Shape: Where a muzzle is placed tightly against the surface o f the abdomen, thorax,
limb, neck, and the wound will be single and circular, of a size approx imately equal to
the bore of the weapon. When the wound is made over a site with underlyin g bone,
especially in the scalp, back of the neck, sternum, shoulder, hip and other areas where
the soft tissues lies thinly over bone, the large volume of discharge gases cannot
dissipate, as they can into the abdomen, chest or mass of muscles, so the gases raises
the skin like a dome in the moment of fire, sometimes producing a muz zle mark. When
the gas volume is large, this dome may then split, causing a cruc iate, stellate or ragged
wound, with skin flaps.
• Soiling and burning: In a tight contact wound, the skin forms a seal around the muzzle,
preventing much escape of hot gas or soot, so that soiling and burning i s minimal or
absent. The clothes may be signed at the edge of the hole and there may be a ring of
burning around the skin wound. Also, where clothing is interposed between the m uzzle
and skin, soot is much more likely to escape sideways and may be found i n each layer
of fabric and on the underlying skin.
• Muzzle impression: There may be a muzzle impression in a tight contact wound made
by firm mechanical pressure or impact of the metal rim against the skin.
36
• Carbon monoxide: Carbon monoxide in the gases combines with haemoglobin and
myoglobin to give a pink coloration to the interior of the wound track and a djacent
tissues.
b. The close discharge of a shotgun (0-15 cm.)
Assuming that the body surface is uncovered, a close discharge-one between actual contact
and about 15 cm – is likely to show the following features:
• singling of the hairs around the wound;
• burning of the skin;
• the tissues within and around the wound may be cherry- pink from absorption of
carbon monoxide;
• the wound will be circular if the weapon is held at right angles to the skin and ellipti cal
if slanted, often with undernet edges on one side;
• there will be “smoke soiling” or “soot soiling” of the skin, from carbon deposition;
• any felt or cardboard wads or plastic cups from the cartridge will be within the de pth of
the wound.
c. Short to mid-range shotgun discharge (15 cm-2 m).
• From about 15 cm to 2 m, considerable variation occurs in the appearance of the
wound. The shorter range will provide a similar picture to that of cl ose discharge, but
the soot soiling diminishes and over 20-40 cm it may vanish. At the upper end of this
range, the edges of the wound will become created and scalloped. Thi s is called the
“rat- hole” or “rat- nibbling” from its resemblance to rodent teeth marks.
• From 2 m upwards, the number of satellite pellet holes will progress ively increase
around the main wound.
d. Mid-to distant range shotgun wounds (over 2 m).
• Once beyond 2 m, there will be no burning or smoke staining, rarely will there be
powder tattooing. The spread of pellets, which usually begins at a meter or two ranges,
increases progressively, the central “rat- hole” diminishing at the same rate.
• At distant ranges, beyond 6-10 m, the central hole may shrink to nothing. T here will be
no smoke, flame or tattooing, and no way of determining discharge dista nce of that
particular weapon, which may be 30-50 m. At such ranges, if the pellet s penetrate the
skin, will be just in the subcutaneous tissues
37
5.3.1.2. Exit wounds
• Are uncommon in the trunk as the energy possessed by each pellet is small because o f
its tiny size and the relatively low muzzle velocity of the weapon. The pellet of ten
penetrates the distal chest wall, but is held up beneath the skin of the further side of t he
trunk.
• In the head, neck, limbs children and small thin adults, we may find an exit wound
which may be extremely large with grass tissue destruction exposed.
5.3.1.3. The internal track
• Is more diffuse than that caused by a rifled weapon, though where t he discharge is
contact or close, the compacted mass of pellets travels as a unit for some distances into
the tissues before dispersing.
• The internal damage caused by a shotgun is diffuse and is caused by direct mechanical
disruption by the gas and shot, which enters at relatively low veloci ty. There is no
cavitation effect, the tissue being physically smashed by the impact of a heavy load of
pellets, and in the case of near discharges, by the large volume of the hot gases.
• Secondary damages are caused by the mass of pellets striking the bone and releasing
fragments that may act like secondary missiles, damaging adj acent tissues and
sometimes emerging to from exit wounds.
5.3.2. Wounds from rifled weapons
Injury from rifled weapons varies greatly according to the velocit y of the projectile, but
there are some common characteristics to all types. There is only one missile in each
discharge, unlike shotguns.
5.3.2.1. Entry wounds
a. Contact wounds
• When a rifled weapon is held firmly against the body surface durin g discharge, the
wound is similar to that from a shotgun. There will be burning and blac kening of the
immediate wound edges, but if the seal between muzzle and skin is ti ght, there will be
little or no sideways escape of flame and soiling unless clothing i s interposed. Within
the wound, there will be some placking with soot in the tissues.
• There is usually an areolar of hyperemia that extends beyond the di ameter of the
muzzle and carbon monoxide will be absorbed by hemoglobin and myoglobin in the
vicinity of the skin wound and in the deeper track. There may be bruising . A muzzle
38
imprint may be formed, due to expansion of the tissues by gas entry which forces the
skin against the end of the barrel.
• If the contact wound is over a bony support, especially the skull, then the same
phenomenon occurs as in shotgun wounds: the muzzle gases entering the subc utaneous
tissues cannot expand by displacing adjacent soft tissues and are reflected from the
bone to raise a dome of gases that often splits the entry hole. The result is a linear,
cruciate or stellate tear that may destroy the original puncture.
b. Close – range wounds
• The wound is circular, the edges may be inverted. Within a few ce ntimeters of base
skin there is likely to be burning of the skin, with singeing of hai rs. Hyperemia around
the wound is usual.
• The soot may be seen around the wound. In addition, they will be tiny burns from
specks of incandescent propellant, the so-called “powder tattooing”. The se may pepper
the vicinity of the entry hole. “Fouling” refers to tiny lesions around the entry wound
caused by fragments of metal expelled by the discharge. These come either from the
surface of the missile or from the interior of the barrel. The se particles will not wipe
off at autopsy, whereas soot soiling can easily be removed with a damp sponge.
• Fragments of the shell case may become detached and blown out of the barrel.
• Minute flakes of unburned explosive or inert filter may land on the sa me area of the
skin; these tend to glisten and may be orange or blue, depending on the manufacturer
(these may indicate the nature of the ammunition and may be matched to that in the
possession of a suspect). Carboxy-hemoglobin and myoglobin will be pres ent in the
wound track in diminishing concentration as the range increases.
c. Medium distance wounds
• Unlike the shotgun, once the discharge of a rifled weapon is greater than a meter, there
is nothing to indicate increasing range, until perhaps the erratic trajectory of extreme
distance suggests maximum range.
• The central entry opening of the entry wound is circular and may be inverted- the
margins are driven inwards by the passage of the missile, but t his feature is often
absent.
• The size of the hole is usually smaller than the diameter of t he bullet, due to the
elasticity of the skin (unless the range is so close that ga s entry contribute to the size of
the defect)
39
• The skin immediately around the central hole is discolored, the so-cal led “abrasion
collar”. This may be only a narrow rim or may be equal in width t o the central defect.
The collar is due to the inversion of the skin during penetration by the missile so that
the sides of the bullet are “wiped” by a tiny tube of skin, the epidermis of which is
abraded by heat and friction. The width of the abrasion collar is det ermined by the
degree of inversion and hence the length of the skin tube.
• The inner edge of the abrasion collar may be black, as a result of he ating effects and of
the rubbing-off the dirt, lubricating oil or grease and metal particle s from the bullet.
This is called the “grease ring” or “ring of dirt”, and may be absent if the missile was
clean.
• There may also be bruising around the wound from mechanical damage to a djacent
subcutaneous blood vessels. No burns, soot or powder may be found beyond a variable
distance that will not exceed a meter in the case of a rif le, and half that distance in a
handgun. An impact at right-angles will produce a circular zone of di scoloration on the
skin, while an oblique angle will result in an elliptical mark.
d. Bullet wounds in bone
• Where a bullet passes through bone, especially the thin bone of the skull, the pattern of
“cratering” may be seen. The initial contact of the missile punches a cle an hole through
the outer table of the skull. When the bullet emerges internally, t he inner table is then
unsupported and a cone-shape plug is detached, forming a crater that is appreciably
larger than the external hole. If the bullet transverses the cr anium and penetrates the
opposite side, the same pattern occurs, this time with the small hol e on the inner table
and the crater on the outside. There are often fractures, sometime s comminuted,
running away from the central hole.
5.3.2.2. Exit wounds from rifled weapons
• The muzzle velocity is important in determining whether a singl e bullet will
completely traverse the body. A high-velocity missile (of the order of 800m/sec.) is
likely to pass right through the body unless it strikes a larg e bone structure like the
spine, large limb bone or base of the skull.
• If a fairly intact bullet emerges, the exit wound is likely to be a small everted
defect, either circular or with torn edges. The classical des cription is of a stellate
wound, with triangle skin flaps at the margin, where the bullet w as pushed out
against unsupported skin. Many wounds may be cruciate or linear, and others are as
40
circular as the entrance wound, which may give rise to some diff iculty in
interpretation.
• Penetration of two parts of the body is quite common, a single mis sile causing
several wounds.
5.4. Firearm damage to internal organs
Usually, there are two categories:
5.4.1. Contusion and laceration from low-velocity impact
where a mass of shotgun pellets and gas strikes tissues or orga n, the damage is
simple a mechanical disruption, with widespread hemorrhage from local vessels.
similar, damage is likely from a low-velocity rifled bullet, though less extensive,
which pushed the tissues apart as it plunges through an organ or muscle
secondary damage may occur from fragmentation of the bone or bullet.
danger for life depends on the target tissues (a wound through the thig h may cause
only temporary disability, whereas the same wound through heart or br ain, may be
rapidly fatal)
5.4.2. Hight-velocity missiles
produce disproportionate damage relative to their diameter because of cavitation
effects. This is particularly damaging in solid organs, such as b rain and liver. The
track may be many times wider than the diameter of the bullet, and may consist of
pulped and hemorrhagic tissue left behind by the pulsating cavitation effect, caused
by the lateral transfer of energy as the missile is passing through.
5.5. Shooting distance estimation
5.5.1. Smooth-bore shotgun
Tight contact discharge over soft tissues:
• single circular wound about the diameter of the muzzle;
• smooth margins;
• often, muzzle imprint;
• blackened edge;
• deep bruising;
• pink tissues;
• wads in wound;
41
• no surrounding smoke soiling unless clothing allows leakage.
Tight contact discharge over skull or bony area:
• as last type, but wound may be ragged and split from gas rebound.
Discharge within a few centimeters .
• circular wound, unless oblique discharge;
• smooth or slightly embattled margin;
• no satellite pellet holes;
• surrounding soot soiling;
• dotted powder burns;
• unburned powder flakes;
• burning of surrounding skin;
• burned hairs;
• pink monoxide in tissues;
• wards in wound;
Discharge from 30 cm.:
• circular “rat-hole” wound with nibbled margins;
• no satellite pellets holes;
• soot soiling may persist;
• powder tattooing present;
• little or no monoxide;
• still burning of skin and hair;
• wads in wound.
Discharge from 1 to 5 m.:
• central “rat-hole” wound;
• satellite pellet holes around periphery;
• no burning;
• no soot;
• may be slight tattooing at 1 m.
• no monoxide;
• wads not in wound at upper part of this range.
Discharge over 5 m:
• diffuse pallet pattern;
42
• probably no central hole;
• no burning;
• no soot;
• no tattooing;
• no monoxide;
• no wads.
5.5.2. Rifled weapons
Tight contact over soft tissues .
• possible muzzle impression;
• circular hole with abrasion collar;
• bruising;
• local reddening from heat and monoxide;
• little or no surface burning;
• little or no propellant soiling or powder tattooing;
Tight contact over underlying bone.
• split or crusader wound;
• local reddening and monoxide;
• little or no surface burning or propellant soiling;
• abrasion collar partly lost on skin tags.
Discharge from less than 15 cm.:
• circular hole with abrasion collar;
• flame burn on surrounding skin;
• burnt hairs;
• soot and smoke soiling (depending on ammunition);
• small punctate burns from propellant tattooing;
• unburnt propellant flakes;
• little or no monoxide in tissues.
Discharge from 15 to 30 cm.:
• no soot;
• perhaps powder tattooing depending on barrel length;
• no monoxide;
• rarely flame burns.
43
Discharge from more than 40 to 60 cm:
• circular hole with abrasion collar;
• no burning, soiling, burned hairs or monoxide.
Far distant discharge at limit of range .
• larger, irregular hole with irregular abrasion rim caused by tumbling bullet;
• no other features.
ATTENTION: test firing must be used to validate the pathological interp retation!
44
CHAPTER 6: REGIONAL INJURIES
6.1. Classification of the regional injuries
head injuries:
• Scalp injuries: abrasion, bruising, laceration.
• Fractures of the skull: linear fractures, ring fracture, pond fracture, spider
web fracture, depressed fracture.
• Intracranial injuries: subcutaneous hematoma, extradural (epidural)
hemorrhages, subdural hematoma, subarachnoid hemorrhages, cerebral
injuries (contusions, lacerations, traumatic intracerebral hemorrhage ,
cerebral edema, coup and contrecoup lesions, concussion.
spinal injuries:
• Compression damage
• Hyperflexion and hyperextension injury
• Spinal cord injury
chest injuries:
• Injuries to the chest wall
• Hemorrhage in the chest
• Infections in the chest
• Pneumothorax
• Injuries in the long
• Injuries of the heart: blunt injuries and penetrating injuries
• Injuries to great vassels: aorta, pulmonary artery
abdominal injuries: blunt injuries and penetrating injuries
injuries to the pelvis and pelvic organs: various fractures, dislocations and
injuries of the pelvic organs
fractures of the face: dentoalveolar fractures, Le Fort I fractures, Le Fort II
fractures, Le Fort III fractures, sagittal run.
fractures of the bones of the extremities:
• penetrating fractures,
• in focal fractures,
• in crush fractures.
45
6.2. Head injuries
1. General aspects, mechanism:
Head injuries are frequent in our days; of all regional injuries, there are mo st
common and most important in forensic practice.
The circumstances in which a head injury may occur:
• assaults;
• work accidents;
• accidents in general: in sport, at home,
Head trauma may be:
• closed-the scalp is not lacerated;
• opened-the scalp is lacerated;
Head injuries may occur by the following mechanisms:
Direct mechanism, with two possibilities:
• Acceleration – when the head at rest is stroke by a moving object . In this
case, we have concordance between the injuries of the scalp, skull a nd
brain, at the place of the impact.
• Deceleration- when the moving head strikes an object at rest. In this case,
there is no concordance between the injuries of the scalp, skull and brain.
We find injuries at the place of the impact, but also injuries in t he opposite
place.
• Joint mechanism- the strike of the head is followed by fall. It is a
combination between the acceleration and deceleration mechanisms.
Indirect mechanism:
• Acceleration or deceleration without impact:-in this case, we fi nd important
injuries at the joint between the spine and the head (for example : whiplash
fracture of the cervical spine produced by hyperextension followed by
hyperflexion of the head, without impact of the head – this injuries i s
frequent in traffic accidents)
• Impact in another region than the head- the injuries intermediated b y the
spine or by the mandible in impacts on the lower limbs or on the chin.
2. Types of injuries
2.1. Injuries of the scalp
The injuries of the scalp may show:
46
• the number of impacts over the head;
• the type of the weapon;
• the direction of the blow;
• the vital character of the injuries.
2.1.1. Abrasion of the scalp
• brush abrasions are less common than in other sites because of the prot ective effect
of the hair.
• impact abrasions from a perpendicular force are imprinted usually to the scal p.
2.1.2. Bruising of the scalp :
• bruising of the scalp may be difficult to detect until the hair has been removed;
• usually, at external examination, the bruise appears like a swel ling of the scalp
(epicranial haematoma )
• bleeding under the scalp may be mobile, especially under gravity. T hus, a bruise or
haematoma under the anterior scalp may slide downwards within hours or minutes,
to appear in the orbit, simulating a black eye from direct trauma. Similarly, a
temporal bruise may later appear behind the ear, suggesting primary neck impac t;
• the shape of an inflicting weapon or object is poorly reproduced on the scal p, due
to the padding effect of the hair;
2.1.3. Laceration of the scalp
• laceration of the scalp has a peculiar from because the scalp i s lying over an
unyielding bony support(the skull). Violent compression will crush the scalp
against the underlying skull, so, a blow from a blunt rod demarcated f ashion, which
may appear like a slash from a sharp instrument. So, a major pr oblem in scalp
injuries is the differentiation between incised wounds and lacerati on from blunt
injury. Close examination will show that the blunt laceration has: bruised margins,
head hairs crossing the wound which have not been cut, fascial strands, ha ir bulbs
and small nerves and vessels in the depth of the wound, tissue – bridges between
the margins of the wound;
• laceration of the scalp bleed profusely, so, dangerous and even fatal bl ood loss may
occur;
• laceration of the scalp may reproduce the pattern of the inflicti ng object. Severe
blows from shaped objects such as hammers or heavy tools may reproduc e the
47
profile of the weapon totally or in part; the most important injury i s the avulsion of
a large area of the scalp.
2.2. Facial lesions
Damage to the face is rarely fatal in itself unless it l eads to bleeding into the air
passages. It is often ancillary to fatal cranial damage, or i t may be the route by which
severe trauma reaches the brain.
The usual range of injuries may be present externally but all d egrees of underlying
damage may also occur in the facial skeleton.
2.2.1. Soft tissues:
• The eye-blow is particularly vulnerable, being exposed during falls and blows. A
blunt impact on the blow splits the skin and may cause a frontal f racture that can
involve the occipital margin.
• The injuries of the skin may be produced by a great number of weapons. A peculiar
type is the injuries produced by the shivers of the windscreen in tra ffic accidents:
multiple cuts on the entire surface of the face, which will lead to vicious scars.
2.2.2. The distal part of the nose:
• Is flexible and often escapes serious damage, the abrasion is common. The bony
bridge of the nose may be fractured. Bleeding of the nose is so important.
• The maxilla and mandible: may be fractured by direct blows and m ay cause
important intra-oral bleeding from associated soft-tissues damage.
2.2.3. Injuries to the mouth and lips:
• the lips may be bruised or lacerated, much of the damage arisi ng from the
compression of the lips against the teeth.
• lacerations and bruises of the gums.
• ruptures of the frenulum inside the upper lip
• injuries of the teeth: contusion (the teeth is fixed, but painful and som etimes colored
in pink), teeth mobility, fractures of the teeth, expulsion of the teeth.
2.2.4. Gross injury to the face:
• mostly in kicking and in traffic accidents, may detach the facia l skeleton from the
base of the skull. The lower part of the maxilla, carrying t he palate and upper teeth,
may be completely separated from the rest of the skull.
• Black eyes- may be the result of:
– direct violence – a simple fall onto the face does not usually cause a black eye
48
– gravitational seepage of blood beneath the scalp from a bruise or lace ration
above the eyebrow
– percolation of blood into into the orbit from a fracture of the anterior fossa of
the skull
• Damage to the ear: the external ear often suffers from blows to the head and is an
obvious target in child abuse. Injuries of the external ear may be:
– bruising and laceration of the pinna
– the root of the ear may be detached from the head in severe trauma
– the ear may be bitten and even partly detached
2.3. Fractures of the skull:
2.3.1. Clasification
Fractures of the skull may be:
• complete: both inner and outer table are fractured;
• incomplete (fissure): only one table is fractured.
Types of skull fractures:
• Linear fractures: are common especially in the weak unsupported pla tes; can be
simple / branched out –“spider’s web” fractures.
• Comminuted fractures may be:
o Depressed: in-bending fractures (the inner table will intruded bec ause of the
outer table into the cranial cavity) and out-bending fracture (fragm ents are
throwed from the interior to exterior -in shot for example);
o Non- depressed fractures .
• Ring fractures: in the posterior fossa, around the foramen magnum, caus ed by fall
from a height onto the feet or onto the top of the head.
• Pond fractures: a shallow depressed fracture forming a concave “pond” (the
fracture may take the shape of the impacting object).
• “Spider’s web” fracture: a comminuted depressed fracture may ha ve fissures
radiating from it;
• Depressed fractures: the inner table will be intruded because of the outer table onto
the cranial cavity.
2.3.2. The mechanics of skull fracture:
Fractures of the skull may be produced by:
• Direct mechanism;
49
• Mediated by the spine, mandible (especially at the base of the skull).
When the skull receives a focal impact, there is a distortion of the shape of the
cranium. The area under the point of impact bends inwards and there mus t
consequently be a compensatory distortion of other areas. Both these intr uded and
extruded areas may be the site of fracturing if the bone excee ds the limit of its
elasticity;
When the skull is deformed, compression occurs on the concavity of the curve d bone
and tension on the convexity. If the latter exceeds the elastic thr eshold, then fracturing
takes place. The inner table will fracture where the skull is indented and the outer table
will fracture at the margins of the deformed area.
In a wider impact, the deformation of the skull is less localiz ed but, where the force is
sufficient, the fractures may be remote from the area of impa ct following lines of
structural weakness.
When severe local impact causes focal and general deformation, a c ombination of
depressed fractures and radial fracture lines may form a “spider’s web ” pattern.
When the focal impact is severe, the depressed fracture may fol low the actual shape of
the impacting object (especially when its surface is under 4 cm.)
Where two or more separate fractures occur from successive impacts and meet each
other, the latter fracture will terminate at the early fracture li ne.
2.3.3. Fractures of the base of the skull
Fractures of the base of the skull may be:
• Direct fractures- rarely (for example: shot in the mouth);
• Irradiated from a skull fracture- the most common.
2.4. Intracranial injuries
2.4.1. Subcutaneous hemorrhage : blood accumulation between the scalp and galea
aponeurotica.
2.4.2. Extradural (epidural) hemorrhage:
bleeding between the inner surface of the skull and the dura mater.
sources:
• the middle meningeal artery or a branch of that artery;
• the longitudinal superior sinus of dura mater.
the usual site is unilateral, in the parieto-temporal area, caus ed by the rupture of a
branch of the middle meningeal artery where the latter is transected by a fr acture line.
50
a minimum of 35 ml blood is needed before clinical signs are appare nt; 100 ml is
usually the minimum associated with fatalities.
the clinical signs are classically those of a latent interva l before sufficient blood
accumulates to cause raised intracranial pressure and consequent re lapse into
unconsciousness. The latent interval may be: few hour (over – acute he matoma); 1-3
days (subacute hematoma); 2-3 weeks (chronic hematoma).
autopsy: the hematoma is seeable as a collection of dark blood with clots when we
remove the calvarium. The brain surface will be flattened under the hematoma and we
may find the usual appearances of raised intracranial pressure.
extradural hemorrhage is never a contrecoup injury, we’ll always find it at the strike
place. Most of them are associated with fractures of the skull, but 15% occur in intact
skulls. Usually, extradural hemorrhage is a traumatic lesion, r arely a pathological one
(in diseases of dura-mater).
2.4.3. Subdural hemorrhage
bleeding beneath the dura-mater.
source: ruptured bridging veins (the most common).
characteristics:
• is much more common than extradural hemorrhage;
• is less often associated with a fractured skull;
• may be a contrecoup lesion;
clinical: only when the bleeding is extensive enough to become either a cortical irritant
or a space-occupying lesion (between 35 and 100 ml) becomes clinica lly apparent, at
100 ml it may cause fatalities.
subdural hemorrhage may be of three types:
• Acute – the lucid interval is 1 to 3 days;
• Subacute – the lucid interval is 3 to 14 days-is has a thick parietal membrane;
• Chronic – the lucid interval is 2 to 3 weeks- it has a membrane w ith two layers:
parietal and visceral (after 12 month the membrane is as thick as the dura itself ).
Autopsy appearance:
• Acute subdural hemorrhage: liquid blood and clots beneath the dura.
• Chronic subdural hemorrhage: gelatinous or though membrane (depending to t he
age of hematoma); the contents are thick but liquid, brown or even straw colored.
51
Subdural hemorrhage may be:
• Traumatic lesion
• Pathological:
o associated with pathological lesions of dura or of the brain (vascul ar
aneurisms, cerebral atherosclerosis);
o usually bilateral;
o without traumatic lesions on the head;
2.4.4. Subarachnoid hemorrhage
bleeding in the subarachnoid space
sources: is has a mixed etiology
• damage to the cortex;
• penetrating injuries of the brain;
• many blunt objects that give rise to extradural or subdural hemorrha ge will be
associated with traumatic subarachnoid bleeding.
Subarachnoid hemorrhage is, sometimes, the result of a natural disea se, especially
rupture of vascular malformation of several types. It may appear at the site of trauma
or completely elsewhere. Blood mixed with the cerebrospinal fluid which dilutes it
makes it less ready to clot and allows more mobility.
In head injuries, death is far more likely to be the result of the other concomitant
associated injuries to the brain substance than to a moderate amount of blood in the
subarachnoid space. But death can be rapid when a profuse hemorrhage occurs into the
subarachnoidian space.
2.4.5. Cerebral injuries
the mechanism of brain damage:
• By direct intrusion- when the skull is disrupted (penetrating weapon, bullets);
• By deformation of the brain in closed head injuries. The change in v elocity – either
acceleration or deceleration- leads to damage of the brain even without impact.
when violent relative movement take place between the brain and the dura forming the
partitions of the cranium, the cerebral tissue may be damage ag ainst both shaped edges
and the flat surfaces of the anatomical suspensor system with the cranium.
when a head falls against the ground, pressure momentarily increas es at the impact
point, but falls to a negative value diametrically opposite. These s uction or cavitations
effects are more damaging to neural and meningeal tissue than pressure.
52
when the head which is free to move is struck by a heavy object, t he brain damage
usually occurs directly under the point of impact. This brain damage is sometimes
termed “coup”. If the head is falling and strikes the ground, it is decelerated and a
“contrecoup” brain damage occurs at a point diametrically opposite the impact point.
This phenomenon is useful in distinguishing blows from falls.
contusion and cerebral laceration may be “contrecoup” or “coup” lesions.
2.4.5.1. Cerebral contusions
brain injury due to disruption of the vessels in the gray or white substance.
producing mechanism: rotation and acceleration. When the head is rota ted by an
impact, the layers of the brain tissue slide over each other at different depths in the
cortex.
autopsy appearances: cerebral contusion is often wedge shaped, blue or red, with the
base on the surface of the brain, tapering away into the deeper l ayers. The hemorrhage
may be diffuse or may be punctuate and is often a matt led pur plish red when confined
to the cortex.
2.4.5.2. Cerebral lacerations
laceration of the cortex is an extension in severity of the contusi on in which disruption
of the tissue may be seen.
autopsy appearances: the cerebral surface becomes fissured, frag ments of cortex may
detach and it coexists with an area of traumatic hemorrhage.
laceration and contusions are more often found in those areas of the brain where the
cortex is more likely to come in contact with irregularities (the temporal lobes and the
orbital surface of the frontal lobes).
cerebral contusion and cerebral laceration are always traumati c lesions, and may exist
at the impact place or\and at the opposite point (“coup” or “contrecoup” lesions)
2.4.5.3. Intracerebral hemorrhage
substantial areas of hemorrhage, either infiltrating the brain t issues or forming
hematomas.
there are common in severe head injuries.
they are accompanied by contusion or laceration.
traumatic intracerebral hemorrhage may be caused by coup or contrec oup mechanism
and it may be situated anywhere within the emisphere.
an intracerebral hemorrhage may be, also, pathological- in old pati ents with
hypertension and cerebral atherosclerosis, for example. When a sc alp injury is also
53
present, it is difficult to decide if the head injury is responsibl e for the cerebral
hemorrhage or whether a sudden “stroke” caused by a natural cerebral hemorrhage
resulted in the fall. The presence of left ventricular hypertroph y, a history of
hypertension and the site of the hemorrhage (thalamus, ponds, cerebel lum, more often
occipital), tends to point a pathological bleeding.
2.4.5.4. Cerebral concussion
a transient paralytic state due to a head injury which is of inst antaneous onset, does not
show any evidence of structural cerebral injury and is always f ollowed by amnesia
from the actual moment of the accident.
concussion is a clinical, not a pathological entity.
true concussion may last for seconds or minutes. If prolonged unconscious ness extends
into hours, days, or longer, there is likely some structural brain damage to occurs.
the cause of cerebral concussion seems to be a temporarily dis rupt of the function of
the neuronal apparatus, with changes in the nucleus and cytoplasm of neurons. C hange
in the composition of the cerebrospinal fluid has been inconstantly re ported. It seems
to be a connection between concussion and rotator movements of the head.
2.4.5.5. Cerebral edema
swelling of the brain tissues.
cerebral edema may be:
• A local phenomenon – around almost any lesion, contusion or laceration, t umor or
infarct.
• Generalized.
cerebral edema is extremely common after a substantial hea d injury, especially in
children
it is the most common cause of raised intracranial pressure.
autopsy features: on removing the calvarium, the dura is tense and str etched, the brain
bulging through the first incision in the membrane. The gyri are pale and flattened, and
the sulci filled, giving the normally corrugated cerebral surfa ce smoothness that may
be seen at autopsy. The ventricles may be reduced to slits by swe lling of the adjacent
white matter.
when cerebral edema is the only intracranial abnormality found at autopsy after a head
injury, the cause of death has to be attributed to the swellin g of the brain, compressing
the vital centers in the brainstem.
54
3. Medico-legal issues in head injuries
Type of death: violent or pathological.
Medical cause of death: the lesions which leads to death. For ex ample: extradural,
subdural, or intracerebral hemorrhage; cerebral contusion, cerebral la ceration, cerebral
edema, subarachnoid hemorrhage, and so on.
The mechanism of injuries- using the aspect and the place of the head injuries.
Number of blows- we can establish the number of the blows according to:
• the number of scalp lacerations is the minimum number of the impacts;
• the number of extradural hematomas;
• the number of the skull fractures.
Succession of the blows – this aspect is clarified according to:
• the intensity of epicranial hematomas;
• where two or more separate fractures occur from successive im pacts and meet
each other, the later fracture will terminate at the earlier fract ure line.
Identification of the weapon: using the aspect of the scalp and skull lesions – depressed
fractures may follow the shape of the impacting object, especial ly when its surface is
under 4. cm2.
The causal relation between the trauma and death- we may find:
• direct relation – the injury itself leads to death;
• direct conditioned relation – between the head injury and the death a
pathological condition exists; without this condition, the death doesn’t appe ar.
Pathological condition may be: hypertension, cerebral atherosclerosi s, and so
on;
• indirect relation – death occurs by a complication of the trauma- an infection,
for example.
Differentiation between vital and postmortem lesions and also betwee n the lethal and
the lesions compatible with life – when there are 2 or more assaulters.
Estimation of postmortem interval.
4. Complications of head injuries
Infection:
• the infection occurs mostly in open head injuries.
• is the most recent complication of the open head injuries. For exam ple:
infection of meninges (meningitis); development of a brain abscess
55
Traumatic epilepsy:
• Is a late effect of the head injuries.
• traumatic epilepsy is due to a cerebro – meningeal scar’ for med after a
cerebral contusion or cerebral laceration with or without fracture of the
brain.
• this complication usually appears like tonic and clonic fits, which m ay be
difficult to differentiate from idiopathic epilepsy.
• traumatic epilepsy appears only after 6 months from the head trauma ,
because this is the necessarily time for meningo-cerebral scar to form.
6.3. Spinal injuries
1. General aspects
Though all segments of the spine are vulnerable to trauma, the cervic al part holds the
most interest for the forensic pathologist, mainly because of its close association with
head injuries and vehicular accidents.
2. Mechanism
Spinal damage may be cause by:
• compressional stress.
• hyperflexion stress.
• hyperextension stress.
3. Types of injuries
3.1. Compression damage:
In fall from height either onto victim’s head or feet;
When the person falls onto the feet the kinetic energy can be tra nsmitted through feet,
legs and pelvis to the spinal column. This can be fractured at one or more points, or the
force may cause the upper cervical spine to impinge on the base of the skull and cause
a ring fracture around the foramen magnum.
A fall onto the head may cause the “burst atlas” injury, wh ere the impact of the
occipital condyles in an axial direction wedge the superior atl antal articulating facets
apart and split the ring of the vertebra.
The posterior arch can be fractured in hyperextension by compression between the
occiput and the posterior spine of the axis.
56
Compression fractures may occur most commonly in the lower dorsal and upper
lumbar zone, particularly.
3.2. Hyperflexion and hyperextension injury:
Are followed by: bleeding into surrounding vertebral muscles, rupture of the anterior
longitudinal ligament, tearing of intervertebral discs and of the annulus fibrous.
Nerve roots may be torn or compressed.
Spinal canal may be narrowed, distorted or even almost obliterated by fracture
dislocations of the vertebrae.
Complications: compression, ischemia, hemorrhage and pulping of the spinal cord.
3.3. Spinal cord injury:
Most damage of the spinal cord arises from intrusion of some part o f the spinal column
into the canal (bony fragments or displacement, ligamentum flavum, disc annulus or
extruded nucleus pulposum).
There may be bleeding into the space outside the spinal dura causin g space-occupying
lesion I the canal that compress the cord.
Bleeding may occur within the dura, either from ruptured vessels or from hemorrhage
in the cord itself.
Hematomyelia and edema may develop without any obvious mechanical def ect at the
level of the spinal column caused by the collision of the cord against the wall of the
canal.
6.4. Chest injuries
Damage can be sustained to either the chest wall or to the contents.
1. Types of injuries
1.1. Injuries to the chest wall:
Respiration is depended on the integrity of the rigid chest wall, w hich can be
compromised by:
Severe mechanical failure.
Penetration of the pleural cavities.
Rib fractures commonly occur but may embarrass respiration when t hey are multiple;
their broken ends penetrate the pleura and lungs or when the pleural and muscular pain
limits respiratory effort.
Rib fractures are most often seen in the anterior or posterior a xillaries lines caused by
falls onto the side.
57
The upper ribs are less often fractured, except by direct violen ce from kicking, heavy
punching or traffic accidents.
The fracture sites almost always show bleeding beneath the per iosteum or the parietal
pleura if the fractures occurred during life.
Attempts at resuscitation especially external cardiac mass age cause extensive rib
fractures in about 40% of the cases.
In infants, especially victims of child abuse, rib fractures are common.
The sternum may be fractured by stamping or other frontal impa cts, but far more force
is necessary than with ribs. If posterior displacement of a fr agment occurs, the
underlying heart or great vessels may be severely damaged.
The flail chest occurs when there are multiple bilateral f ractures of most of the ribs and
also of the sternum. The rigidity of the rib cage is lost and a ttempts at expanding the
thoracic volume during inspiration are impaired. The loose section is sucked inwards
during inspiration, this clinical sign is called paradoxical respir ation. Dyspnea,
cyanosis may develop and extreme degrees of flail chest are in compatible with life
because of progressive hypoxia.
The flail chest is caused by:
• Frontal impact in motor vehicle accidents where the victim is thr own against the
steering wheel or dashboard.
• In stamping accidents where the shot foot is applied violently to the supine body.
In any substantial chest injury, broken rib ends may be displaced inw ards, the jagged
tips ripping the parietal and visceral pleura. This may cause a pneumothorax or
hemothorax, or both with the formation of bronchopleural fistula.
1.2. Hemorrhage in the chest
Any injury to the chest wall or lung surface that breaches bl ood vessels and the pleura
can lead to hemothorax.
Intercostals and less commonly, mammary arteries can bleed int o pleural cavities but
most massive hemorrhage comes from large vessels in the lung or mediastinum.
The lung hillum can be torn or penetrated by stab wounds. Another sour ce of
hemothorax is the heart itself, though there must also be a defect in the pericardial sac.
Several liters of blood may accumulate in the chest, either as liquid or clot, or both.
Death may occur from loss of circulating blood volume even if ther e is relatively little
external bleeding.
58
1.3. Infection in the chest
Infection following a chest wound is uncommon in forensic practice as most deaths
occur from hemorrhage within a relatively short time before infection sets in.
Cellulitis, pleural inflammation and empyema may supervene due t o use of some dirty
weapon or clothing or some foreign material being carried into the wound.
1.4. Pneumothorax
A common traumatic cause of pneumothorax is a stab wound of the chest that allows
direct communication with the exterior, though usually the layere d skin and
intercostals muscles closes the track when the weapon is withdrawn.
Natural diseases such as a ruptured emphysematous bulla, a tubercul ous lesion at lung
periphery or a tear at the site of fibrous pleural adhesion can also cause pneumot horax.
There are three types of pneumothorax:
1. Simple pneumothorax : where a leakage through the pleura allows air to enter
the pleural cavity but where the communication rapidly closes. The lung partly
collapses, but if death does not supervene, the air is soon absorbed. If the
communication remains open, then a bronchopleural fistula ensues with air in
the pleural cavity, but as it is not under pressure, it will bubble out at autopsy
when “water test” is attempted. Radiology is the best to demonst rate this type
of pneumothorax.
2. Tension pneumothorax : when the leak in the pleura or rarely the chest wall
has valve-like action, air is sucked into the pleural cavity at eac h inspiration,
but cannot escape on expiration. This pumping action leads to a tension
pneumothorax, which causes complete collapse of lung onto its hilum and a
mediastinal shift to opposite side. This type can be demonstrated a t autopsy by
penetrating an intercostals space under water and also by radiolog ical
examination.
3. When an injury of the chest wall communicates with the pleural cavi ty, a
“sucking wound” may form with direct passage of air from the exte rior. This
type is seen in military surgery and is complicated by hemorrh age and
infection.
1.5. Injury of the lungs
Bruising of the lungs, can occur in open as well as closed injuries to the chest.
Any substantial impact on the chest can contuse the lung surface or deeper parts.
59
Deceleration injuries are seen in falls and traffic accide nts commonly along the
postero-lateral surfaces where a vertical line of subpleural br uising occurs. The outline
of the ribs may be imprinted in lines of contusion on the pleural surface of the lungs.
Severe bruising may cause subpleural blood blisters.
In all severe chest injuries the central parts of the lungs may show bleeding with actual
hematoma formation.
Laceration of the lungs: can result in blunt injuries with detachment of lobes or parts of
a lobe. The hilum may tear and the pulmonary ligament below the hilum is a frequent
site of hemorrhage.
Penetrating injuries of the lungs are commonly produced by knives. The w ounds may
penetrate lung parenchyma, large vessels or may be “through a nd through” causing
severe damage to heart and great vessels.
1.6. Injury of the heart
1.6.1. Penetrating injuries
A common form of homicide is a stab wound of the chest which penetrate s the heart.
Sometimes the sternum is penetrated by a forceful blow that rea ches the underlying
heart but most stab wounds enter via the intercostals spaces, or through a rib or costal
cartilage.
Rarely, an upward stab from the abdomen reaches under the costal marg in to penetrate
the diaphragm.
The right ventricle is often injured by stab wounds as it presents the largest frontal
area, but the anterior interventricular septum and the left ventricle are als o vulnerable.
A shallow stab wound may enter the myocardium and not reach the lumen of the
ventricle. In such a case there may be little disability unle ss a coronary vessel is
severed, which may either cause death from myocardial insufficie ncy or cardiac
tamponade.
In the thin right ventricle the knife passes into the cavity lea ding to copious bleeding in
the pericardial sac even though the intraventricular pressure is r elatively low because
of the inability of the thin wall to close the defect by muscle overlap and contra ction.
Whereas in the left ventricle, the contraction of the layered thic k wall may partly or
wholly seal the wound and bleeding can be slight. It is, however, more c ommon for
persistent bleeding to occur and, if the drainage from the pericardia l wound is less than
the leakage from the ventricle, eventually a cardiac tamponade may occur.
60
1.6.2. Blunt injuries
Are seen in road traffic accidents, falls from height and in stamping assaul ts.
There are usually multiple rib and sterna fractures with or without flail c hest.
Occasionally there can be heart damage in an intact chest cage.
Fatal blunt damage of the heart may occur, without a mark on the ski n of the thorax
nor damage to the rib cage.
The cardiac injuries are usually seen on the front of the organ, espe cially to the right
ventricle.
Rarely posterior bruising and laceration can occur if the heart is compressed aga inst the
thoracic spine as in stamping assaults and steering wheel impacts.
In gross injuries such as aircraft crashes the whole heart may be avulsed fr om its root.
1.7. Injuries to great vessels
1.7.1. Injuries to aorta
Is the most vulnerable vessel that suffers injury in decelerat ion trauma from both road
and falls from height.
When the thorax is suddenly decelerated, the heart being relatively mobile in the chest,
attempts to continue in the original direction. This causes severe traction on the root of
the heart with complete or partial rupture of the aorta in the descending part of it s arch.
In falls from height, the lesion is the result of abdominal and thorac ic viscera being
forced caudally by the abrupt deceleration while landing on the feet or buttocks.
Rupture commonly occurs almost constantly at a point 1,5 cm. distal to the attachment
of the ligamentum arteriosum.
The lower thoracic aorta is closely bound to the anterior longitudinal ligament on the
front of the dorsal spine, until it reaches the termination of the ar ch, where it curves
forwards. This appears to be the weak point and transaction occurs at this level,
sometimes so cleanly that it looks like a surgical incision. The tear is annular and at
right angles to the axis of the aorta. Sometimes, there may be multiple parallel intimal
tears near the main transaction, called the “ladder-rung tears”.
1.7.2. Injuries to pulmonary artery
May be damaged by depressed rib cage and sterna fractures in stamping assaults and
steering wheel impact in vehicular accidents.
The great vessels are often involved in penetrating injuries.
61
6.5. Abdominal injuries
1. Closed/blunt injuries
Are common from both vehicular accidents and assaults.
They can occur in:
• Impact of the abdomen by a car steering wheel, the liver, inte stine and mesentery
are most vulnerable.
• Crushing between two vehicles, or between a vehicle and a wall.
• Railway and industrial accidents where squeezing between two opposing surfac es.
• Homicides, assaults and child abuse, kicking, stamping and heavy punching.
• Fall from heights.
2. Open/penetrating injuries
may result from cutting or stabbing weapons, firearms, horns and c laws of animal or
fall over sharp projecting object.
3. Someothers types of injuries
• Bruising of the abdominal wall both of the skin and the underlying muscles.
• Extensive bleeding into peritoneal cavity from rupture of a parenchimatous organs.
• Bruising, rupture or penetrating injuries of the stomach and diaphragm.
• Extensive bruising of the gut and its vascular mesentery.
• Rupture or penetrating injuries of the spleen, liver, kidney.
6.6. Injuries to the pelvis and pelvic organs
In severe trauma, the pelvis undergoes various fractures as well as dislocati ons:
Where great pressure is applied to the front of abdomen or pubic area a s in running
over by a vehicle wheel, the pelvis is splayed open, symphysis s eparates and one or
both sacroiliac joints becoming dislocated.
When an impact occurs from the side, superior and inferior pubic ramous are fractured
with dislocation of sacroiliac joint.
In circumstances of fall from height onto the feet, due to the trans mission of force up
the legs, both the sacroiliac joints may dislocate and even one or bot h femoral head
may be driven into acetabulum. When the hip joints remain intact, the pe lvic girdle
may fracture and sacroiliac joints may dislocate.
Due to a kick or heavy fall on to the base of spine, fracture of s acrum or coccyx may
result.
62
Empty bladder is rarely injured in trauma but a full bladder gets injured from blows,
kicks and other blunt trauma. Other pelvic organs are quite protected fr om blunt
injuries.
External genital may suffer injuries especially scrotum is quite vulnerable to severe
bruising resulting from kicks. Scrotum and vulva may suffer injuries f rom falling
astride on objects and in vehicular accidents.
6.7. Fractures of the face
Are produced by assaults and motor vehicle accidents.
Classification:
1. Dent-alveolar: direct force applied anteriorly or laterally c auses separation of a
fragment of the mandible.
2. Le Fort I: a transverse fracture of the maxilla, above the api ces of the teeth,
through the nasal septum and maxillary sinuses, the palatine bone and the
sphenoid bone.
3. Le Fort II: has the same path posteriorly. As it proceeds anteri orly, however, it
curves upward near the zygomatic-maxillary suture, through the infe rior orbit
rim onto the orbital floor, through the medial orbital wall and across the nasal
bones and septum.
4. Le Fort III: is a high transverse fracture of the maxilla t hat goes through the
naso-frontal suture, through the medial orbital wall and fronto-zygomati c
suture, across the arch and through the sphenoid.
5. Sagittal run in a sagittal plane through the maxilla.
6.8. Fractures of the bones of the extremities
1. Fractures from direct application of force:
When a blunt object impacts a long bone, it tends to bend the bone, producing
disruption or cracking of the bone on the convex or tension side which is opposite the
impact.
If the force of impact is severe there is also a crushing on t he side of the bone to which
the force is applied.
In comminuted fractures, the bone in broken in many fragments.
2. Classification of fractures caused by direct application of force:
depends on the amount of force applied to the bone and the size of area to which it is
applied:
63
Penetrating fractures are caused by large force acting on a small area, for example
fractures caused by bullets.
In focal fractures:
• A small force is applied to a small area (are seen in forea rms when an
individual has tried to ward off blows a bat or pipe).
• The fracture is usually transverse.
• Minor injuries of the adjacent soft tissues soft (an abrasion, contus ion, or
small laceration).
• In areas where two bones are adjacent to each other (the forea rm or calf
region), typically only one bone is fractured.
In crush fractures:
• A large force is applied over a large area (fractures of t he legs in motor
vehicle – pedestrian accidents)
• Extensive soft tissue injuries.
• Comminuted fractures of the bone.
• In the forearm and lower legs, there is usually fracture of both bones at the
same level.
In severe impact injuries of the legs, a number of possible fract ure patterns can be
produced (transverse; oblique; spiral; segmental; comminuted; longitudi nal split;
tension wedge; compression wedge).
Fractures caused by indirect application of force are produced by a force acting at a
distance from the fracture site.
3. Other classification:
Traction: the bone is pulled apart by traction (violent contraction of the quadriceps
muscle with resultant transverse fracture of the patella).
Angulation: the bone is bent until it snaps. The concave surface is c ompressed and
the convex surface is put under traction resulting a transverse fracture.
Rotational: the bone is twisted and a spiral fracture is produced.
Vertical compression: produce an oblique fracture of the body of long bo nes, with
the hard shaft of the long bone driven into the cancellous end.
Angulation and compression: the fracture line is curved, with an oblique
component due to compression, and a transverse component due to angulation.
64
Angulation, rotation and compression fractures: the angulation plus rotat ion
produces an oblique fracture, with the compression increasing the tendency toward
fracture.
4. Someother classification:
Opened fracture – the fracture is accompanied by a wound in the skin.
Closed fracture – a simple fracture with no open wound.
65
CHAPTER 7: FALLS FROM HEIGHT
7.1. General aspects
Fall is dropping down from a height of relatively high position due to force of gravity ;
During fall the potential energy due to height is converted to kineti c energy under the
influence of gravity;
At impact some of the energy is imparted to the body resulting in injuries;
Falls may occur at the ground lever or from some height.
We may distinguish two types of falls:
falls from a standing position;
falls from heights.
7.2. Falls from standing position
Circumstances:
• drunken person;
• assault;
• illnesses such as faint, stroke, epilepsy, etc;
• slippery ground;
• obstacles;
• darkness.
Causes of falls from a standing position:
• lack of poise;
• lack of consciousness;
• pushing.
The typical lesions in falls from standing position are injuries only on prominent parts
(nose, chin) and only on one side of the body.
If the person is conscious, the injuries are not so serious: bruises, abrasions, lacerations
on the prominent parts, sometimes fractures of the upper or inferior limbs.
Falls in old people may frequently cause fractures of the post-cra nial skeleton-
especially the neck of the femur, though ribs, arms and pelvis may a lso suffer.
Osteoporosis is the major reason for the large number of such injuries from falls .
If the person is unconscious (falls after a fit, faint, stroke) the injuries are more serious
and death may occur. In these cases death may occur as a result of a head injury,
especially onto the back of the head.
66
In cases of falls with cranial impact, often contrecoup lesions ma y occur (contusions,
cerebral lacerations). For example, an occipital impact produce frontal contrecoup
lesions. We may also find a subdural or extradural hemorrhage.
Ruptures of internal organs (liver, spleen) may occur on the pathol ogical organs or if
the victim is falling on sharp objects.
7.3. Falls from heights
Falls from a considerable height are common in suicide and in acci dents (especially in
children). Occasionally homicide may occur, especially in children.
The body may fall maintaining the same orientation to the ground or may turn and
twist in the air. This means that the body may strike the ground i n many different
attitudes. The victim may also strike some obstacles on his way down.
The seriousness of the injuries depends on the height of the fall.
The primary impact is usually the site of the most severe injuries; the body may also
strike two areas simultaneously, such as the head and shoulders.
If the body is falling onto the head, a massive fracture may be p roduced and often a
scalp laceration and sometimes extrusion of the brain. Both vault a nd base may be
fractured and sometimes the base is driven down over the cervical spi ne, the latter
projecting into the posterior fosse.
If the primary impact is on the feet, the impact is transmit ted up the spinal column and
the cervical spine projects into the posterior fosse producing a “ri ng fracture” around
the foramen magnum of the occipital bone. This kind of fracture occurs only if the legs
are not fractured.
When the fall occurs on to the feet, the legs may be broken at any level, at tibia or
femoral level, often bilaterally.
When the fall occurs onto one side of the body, any combination of injuri es may
occurs:
• multiple rib fractures;
• shoulder or arm fractures;
• lacerations of the back, buttock or ribs;
• severe abdominal or thoracic injuries with internal lesions: rupture of the liver,
spleen, lungs, heart.
67
7.4. Forensic issues in falls
The type of death: may be violent or pathological (in strokes due to a disease followed
by fall).
Medical cause of death: traumatic shock, hemorrhagic shock, ruptures of internal
organs, head injuries.
The conditions that leaded to fall:
• external conditions: environmental factors (darkness, slippery ground,
obstacles);
• internal conditions- diseases with lack of consciousness (epilepsy) or
alcoholism;
The level of alcohol in blood and urine.
Juridical form of death:
crime;
accident: the most frequent;
suicide: especially the persons with psychiatric diseases (ch ronic alcoholism,
melancholy, etc);
dissimulation of a crime – throwing the body from a height trying to dissimulate
the lesions produced by aggression. We may differentiate the vital r eactions of
the lesions produced by aggression from the falling lesions without vita l
reactions.
The causal connection between the trauma and death.
Differentiation between fall and assault.
Differentiation between vital lesions and postmortem lesions.
68
CHAPTER 8: TRANSPORTATION INJURIES
8.1. Road traffic accidents
In developed countries, road traffic accidents represent the most com mon cause of
death below the age of 50 years.
The type of injury varies according to the position of the victim in the accident:
• car driver;
• passengers: in the front seat or in the back seat;
• motorcyclist;
• bicyclist;
• pedestrian.
8.1.2. Injuries of the vehicles occupants
Tissue injury is caused by a change of movement rate, if meani ng acceleration or
deceleration. The change movement rate is conveniently measured i n “gravities” or “G
forces”. The value of a G force may be calculated with the formula:
G= c ( v ) D, where:
c= a constant (0,0039);
v= velocity in km/h;
D= the stopping distance after impact measured in
meters.
Deceleration of the order of 300 G can be sustained without injury.
8.1.2.1. The driver
8.1.2.1.1. Frontal impact – is the most common event.
The unrestrained driver slides forward, so his legs strike the fa scia and his abdomen or
lower chest contacts the lower edge of the steering wheel.
Impact against the fascia cause abrasions, lacerations and frac tures of the legs around
knee or upper stein level.
The impact of the abdomen and chest against the steering wheel may cause:
• fractures of the ribs and sternum;
• hemothorax or pneumothorax;
• bruising or laceration of the lungs;
• cardiac contusion or laceration;
69
• rupture of the liver (50%);
• rupture of the spleen (36%);
• rupture of aorta.
The head goes forward, and there is a flexion of the cervical and thoracic spine s. In this
case we may observe fractures of the cervical or thoracic spine.
The head may strike the windscreen, the upper windscreen rim or the side pillars. In
this case, scalp lacerations, abrasions, contusions, fractured skull, brain damages may
occur.
The face often suffers multiple cuts from contact with the shattered safet y glass.
Often, the windscreen is perforated by the head or face and the w hole body may be
ejected through the broken glass on the bonnet or on the roadway ahead.
Ejection injuries are often lethal, the victim has multiple injur ies, either from the
contact with the road surface or from being struck by other vehicles.
The engine or front-wheel may be forced back into the passenger compartment
intruding upon the driver (if the impact is strong ).
The control pedals also take part in intrusion and, in the usual despera te braking; the
reflex pressure of feet on rising pedals and floor may occur trans mitted force up the
legs and into the pelvic girdle.
Pressure of the feet on the floor, especially when it is intruded by the engine, may
causes fractures anywhere from foot to femur.
The steering column may crush the driver’s chest or abdomen. Modern design has
reduced the danger by making the column telescopic, but injuries sti ll occurs-
sometimes from the wheel itself breaking and penetrating the chest.
The door may burst open and the driver, if unrestrained, is ejected on t he road,
especially in a crash that has a roll-over component.
Upper limb injuries are lees common, but may occur from transmitte d force through
gripping the steering wheel or from impact against the wind – screen, pillars, bonnet or
ground.
8.1.2.1.2. Rear impact
The driver is violently pushed and severe hyperextension of the neck occ urs. If it is a
front obstruction, the hyperextension is followed by deceleration wit h flexion of the
spine and the “whiplash” fracture of the spine occurs.
70
8.1.2.1.3. The side impacts
The injuries depend on the amount of intrusion of the driver’s door and side panels.
8.1.2.2. Front seat passenger
The front passenger seat is the most dangerous place in the car (“la place du mor t”).
We may find the following injuries:
• injuries to the knee region from contact with the fascia;
• the projection through the windscreen may produce lacerations of the face;
• whiplash injury to the cervical and thoracic spine – due to rapid acce leration
and deceleration;
• frontal or parietal head injuries from contact with the windscreen pillar;
• cuts upon the face from shattering of safety glass;
• projection on the road, with secondary injuries, due to other vehicles or by the
fall, usually with lethal lesions (the most dangerous on the head)
It is notable that the safety belts and harness have reduced mort ality, mainly from
preventing ejection into the road, the most frequent cause of death f or the front seat
passenger. For example: man and wife in the car, an accident produc es and the car falls
in a hole. The man is perfectly healthy because he uses the seatbelt, but the woman
falls by the burst door and dies.
8.1.2.3. Rear seats passengers
The often have not severe injuries due to the absence of the windscr een and fascia and
the cushioning effect of the front seats.
Rear seat passengers may present:
• injuries from contact with the door handles, interior lights, etc;
• ejection on the road through bursting doors with secondary injuries due to
striking the road or hitting by other vehicles;
8.1.2.4. Seatbelt injuries
It is uncontested that their use reduces death and serious injury by a factor of 20-25%,
but the seatbelts may causes injuries by themselves, sometimes of considerable
severity.
when the person is too small for the seatbelt, such as a child or a small woman, the
body may slide from under the seatbelt and it may act as a garrote around the neck.
pregnant women have problems with belts, with uterine and fetal injuries.
bruising is the most common injury, under the belt, in the abdominal or chest wall.
71
fractures of the ribs.
fractures of clavicle or sternum when the belt crosses them;
the lumbar spine suffers a compression, with fractures or the disc may be dislocated,
also the posterior arch, pedicles or transverse processes may be damaged.
the abdominal contents suffer most, especially the rupture of the me sentery or the
small or large intestine due to the flexion of the body on the sea tbelt. The abdominal
aorta may be crushed.
the seatbelts impede escape from a burning vehicle but fires invol ving passenger car
crashes are quite rare.
8.1.3. Pedestrian injuries
Pedestrian injuries are the most common road fatalities, accounting for 50% of t he road
deaths each year.
The most exposed are old people and children.
The causes of accidents are:
• moving into the road-way after alighting from buses;
• moving out between parked vehicles;
• the high speed of the motor vehicles.
It is certain that the mechanism is only acceleration (not a deceleration pr ocess).
The pedestrian injuries are divided into primary injuries and secondary injuries from
the contact with the ground or other stationary objects.
The impact may be frontal, from the rear or from the side (the most common).
The usual sequence of events is as follows: – the bumble bar (the further most
projecting part of the vehicle) strikes below the center of gravit y of the adult
pedestrian, which lies in the abdominal region. Thus, the first impact is on the legs to a
height from the ground depending on the type of vehicle – we may find a brasions,
contusions or fractures beneath the knee or on the thigh, on the abdomen, arms or head
(trucks)
After the impact, depending on the profile of the front of the car, the struck pedestrian
may be:
• thrown forwards in the direction of travel if the bonnet-front is high and blunt;
• scooped up onto the bonnet top, he can be thrown on the ground in the back of the
car or on the bonnet of another car coming from the back.
72
• if the pedestrian is thrown forward, secondary injuries will be t he result of striking
the ground: fractures of the skull, ribs, pelvis, arm or thigh. We may find also
another type of injuries: abrasions, contusions, lacerations.
We must measure the distance from the heel to the lesion for the identification of the
vehicle.
At children’s, the first impact is, usually, on the thigh with fem ur fractures, at the
abdomen, chest, arms or head.
Traffic accidents are the most frequent cause of skull fractures, especi ally of the base.
Fractures of chest, arms and pelvis and injuries of the abdomen follow frequency.
Often, the injuries are concentrated on one side, usually on the opposite side of the
point of primary impact because the body was thrown down onto the road.
Also the pedestrian thrown on the road may be hit by another vehicle.
If the pedestrian is thrown on the bonnet, he will have injuries es pecially on the head
from the contact with the windscreen pillars (the contact is rar ely midline), with skull
and base fractures, brain injuries, cuts upon the face and chest f rom the shattering
glass.
When a wheel passes over the pelvis, abdomen or head, there may be grea t internal
damage with little surface injury. The wheel may pass over t he head, crushing the
cranial vault, often the brain being extruded through the scalp lacerations.
It is possible that the skin to be rolled off in a flying-type injur y, revealing the muscle
beneath over a wide area.
On the clothes of the pedestrian, we may find glass fragments, grease or paint marks.
These are very important for the identification of the vehicle in a “hit and run”
accident.
In motor vehicle accidents is very important to take blood samples f or determination of
the level of the alcohol in the blood and the blood group.
The mechanisms involved in the pedestrian injuries are:
the strike, followed by the thrown of the victim forwards on the ground or on
the bonnet of the car;
the wheel passes over the body- the trace of the tire is usuall y imprinted on the
skin or on the clothes of the victim;
the compression of the body by the vehicle, frequently with dragging the body;
the dragging of the body- with characteristic lesion – abrasions li ke parallel
lines.
73
In traffic accidents, these mechanisms are associated.
A lethal traffic accident may be possible at any speed: the f irst lethal traffic accident
was in England in 1896 at a speed of about 6 km/h.
8.1.4. Injuries to motorcyclists
In developed countries, the rate of injury and death amongst motorcycli sts is far higher
than among car drivers.
The two extremities of the body suffer most in motorcycle acc idents, but also it is a
high injury rate for chest and abdomen.
All types of injuries may be present to the motorcyclists.
In the high-speed impact of a motorcycle, we may find:
• primary injuries – the result of the initial contact;
• secondary injuries – from striking the ground.
The primary injuries are often on the legs, with abrasions, bruises, laceratio n, fractures.
The secondary injuries are the result of the impact with the road surface:
• skull fractures at any part of the head, but often temporo – parieta l, with brain
injury and with contre – coup brain injury;
• the fracture of the base- the extension of the skull fracture to the base- typical
for motorcyclist accidents;
• the ring fracture around the foramen magnum, in the posterior fosse, ca used by
an impact on the crown of the head;
Usually the fatal injuries are the lesions of the head, especial ly of the brain. The use of
crash helmets has reduced fatalities but at high speed, no protection will be acti ve.
The legs may be damaged by the secondary impact with the ground: a brasion, bruises,
laceration, fractures. Any part of the body may suffer an injury, but less often than the
extremities: ribs, limb fractures, rupture of the liver and spleen.
8.1.5. Causes of death in road traffic accidents
The most frequent cause of death is the injury of the head: fract ures of the skull and
base with different degrees of brain damage.
The rupture of aorta or lesions of internal organs with internal or external massive
bleeding.
Multiple rib fractures with an acute respiratory insufficiency.
also death may be produced by complications like:
• Infections (bronchopneumonia)
74
• Fat embolism (from a fractured femur)
• Pulmonary, myocardial or cerebral infarction, etc.
The presence of natural diseases is very important in all traf fic death, as a possible
cause of contribution to the accident- for the pedestrian and also for the car driver.
Also drug or alcohol intoxication may represent the cause of the ac cident especially in
pedestrian victims or drivers.
8.2. Train accidents
We may find three main situations:
1. Lesions of the passengers in the train crushes.
2. Lesions of pedestrians hit by train.
3. Lesions of passengers falling out from train.
8.2.1. Lesions of the passengers in train crushes
May happen in train crushes, when the number of victims is high and l esions are
important because most of the train crashes are frontal.
In most of the cases, the vans are turning over, victims hitting the walls, windows and
luggage supports.
Victim from the first van have more important lesions, because this van is usually
together with the locomotive.
The variety of lesions is important, starting with bruises and endi ng with fractures and
body fragmentation.
Lesions are dispersed all over the body, without any order.
8.2.2. Lesions of the pedestrians hit by the train
We can have different circumstances:
8.2.2.1. Accident
this is the most common situation found in medico-legal practice;
the pedestrians may be hit when they cross over the rails or when t hey are near a
moving train;
the injuries, of all degree, may be found all over the body and- if the victim is treat
with the wheels of the train – the body is fragmented and the part s of it are carried
along a big distance from the place of the accident.
8.2.2.2. Suicide
The person lays with the neck on the rail (in this case, the person i s beheaded) or with
the abdomen on the rail (in this situation, the section of the body at this level occurs)
75
For sustaining a suicidal circumstance, the following aspects are importa nt:
• other suicide attempts, by other methods, in the past;
• mental disorders;
• finding any letter for the family, friends, in which the victim motivates the
suicide;
• no violence signs by another means than the train induced injuries.
8.2.2.3. Murder
The victim may have the legs or the hands tied.
The forensic pathologist may also find other violence signs, induced b y other methods
(for example strangulation mark )
8.2.2.4. Dissimulation of a murder
Some criminals try to hide their murder by seating the corpse on the rails.
In this situation, the lesions induced by the train have no vital react ions (hemorrhagic
infiltration) and lesions with vital reactions, induced by other met hods may be found
(for example strangulation mark).
8.2.3. Lesions of passengers falling from the train
The passengers may falls from the train accidentally or bein g pushed by another
person.
After the passenger fall from the train, the body is turning on the impact plane, so the
lesions (of all degrees of gravity: bruises, abrasions, wounds, fract ures, damages of the
internal organs) are found all sides of the body.
There are situations when the person fall from the train under the w heels; in this case
the body is fragmented and parts of it are carried on large dis tance from the accident
place.
A peculiar situation is that of the passengers traveling on the r oof of the train. They
may be hit at the entrance in tunnels, suffering usually lethal inj uries at the face or on
the back side of the head. They may be also beheaded by the electri c cables, if they are
standing.
8.3. Plain accidents
Plane accidents may occurs in the following circumstances:
In the air.
Crush between two planes.
Desertion of the plane.
76
At the take – off or landing moment.
Plane accidents have a great gravity, usually without any survivor s, especially when
the accident occurs in the air.
The bodies of the passengers and of the crew members are broken up, mut ilated,
burned; that’s why an identification activity is usually necessar y. From this reason, a
multidisciplinary team must arrive at the scene of the crush. T his team is made up of
police members, forensic pathologists and odonto-stomatology specialists.
The activity of identification of the victims in a plane accident have two stages :
At the scene of the crush: the team must observe and note:
• The diameter of the surface covered by the human remains – accordi ng to
this surface, the forensic pathologist can determine the high from w hich the
plane fell.
• The position of each body or body fragments.
• Observing and collecting all identification act or personal object found
under or around each body.
• Each body or fragment is numbered and photographed.
• All the bodies are transported to a central morgue, where the se cond stage
of the identification activity starts.
At the morgue:
• The main identification method for the victims of a plane accident i s the
stomatologic identification. The teeth are examined and the dental f ormula
is carried- out; the identification consists of comparing the dental formula
with the stomatologic file of the person. In Romania, that comparis on is
sometimes impossible because the majority of people do not have a
complete stomatologic file during their life the method is very good for the
members of the crew who have for sure a stomatologic file.
• The fingerprints: is also a very good method but, to be used, evidence of the
dead person’s fingerprints must be available.
• Another identification method is using the identity papers, the person al
objects found at the scene of the accident – in this case, collaborat ion with
the family of the victim is very important.
• Anthropologic identification is carried out when only bony remains are
found at the scene of the accident.
77
CHAPTER 9: MECHANICAL ASPHYXIA
9.1. General aspects. Definition. Classifications
Asphyxia is an old term and also a wrong one. It means “lack of pulse” and it was used
because in the past existed the idea that blood vessels were full with air not with blood.
The correct term is “hypoxia” (for diminished oxygen concentrati on) and “anoxia” (for
the complete lack of oxygen).
9.1.1. Definition:
– mechanical asphyxia is represented by violent contribution anoxic states.
9.1.2. Classification:
– there are many classifications of anoxic states.
9.1.2.1. Contribution anoxia
when the passage of oxygen to pulmonary alveoli is blocked. The blockage may be
anywhere at either pharyngeal, laryngeal, tracheal or bronchial level.
Contribution anoxia may be:
Violent (mechanical asphyxia) in the following cases:
• Insufficiency of oxygen in the breathed air or replace of the oxyg en with other
gases.
• An obstacle on the respiratory ways, due to:
• compression of the respiratory ways: hanging or strangulation (wi th
the hand or with a ligature)
• obstruction of the respiratory ways: suffocation and drowning.
• Insufficiency of the respiratory movements in thoraco-abdominal compression.
Pathological :
• Obstruction of the respiratory ways due to tumors, or edema of the larynx.
• Insufficiency of the respiratory movements due to central nervous system
diseases for example.
• Failure of the gas changes between the alveoli and the blood vessels
(pneumonia for example)
9.1.2.2. Transportation anoxia
when a reduced ability of the blood to transport oxygen occurs.
Transportation anoxia may be:
78
Violent:
• carbon monoxide intoxication when the oxygen is replaced by carbon
monoxide.
• severe trauma with a great internal or external hemorrhage;
Pathological :
• cardiac insufficiency;
• severe anemia;
9.1.2.3. Utilization anoxia
the impossibility of the peripheral cells to use the oxygen.
utilization anoxia may be:
Violent : Example – cyanide poisoning, where the cytochrome – oxides enzyme
system of the cells are inactivated.
Pathological : Example – alkalosis or acidosis states that appear in cardi ac or renal
insufficiency.
9.2. Autopsy features
9.2.1. General signs:
9.2.1.1. General external signs:
The lividities are bluish and disposed on a big surface- because of the great quantity of
reduced hemoglobin in the blood.
Cyanosis of the lips, ears, sometimes of the whole head and of the nails.
On the lividities and also on sclera or conjunctivae, we may find pet echial
hemorrhages (small pin-point collections of blood).
This kind of petechial hemorrhages may be found also on the visceral pleura, so called
“Tardieu’s spots”. Petechiales are caused by an acute rise of the venous pressure that
causes over distension and rupture of thin-walled peripheral veins es pecially in lax tissues
(eyelid) and in unsupported serous membranes (pleura, epicardium). Petec hial may occur
also on the internal face of the soft tissue covering the skull, in the brain (especially in the
white matter); there may be large patches of bleeding in the subarachnoid spac e.
9.2.1.2. General internal signs
Petechial hemorrhages on visceral pleura, epicardium, internal face of the soft tissue of
the head, in the white matter of the brain.
79
Liquid bluish blood. The blood is bluish due to the big quantity of reduced hemoglobin
in the blood and is liquid because of the great quantity of carbon dioxide in the blood
which hinders blood coagulation and because of the rapid death.
The right heart is dilated due to the big pressure in the pulmonary circulation.
Stasis in all internal organs.
The most important changes are in the respiratory system: pulmonary edema,
pulmonary stasis, pulmonary emphysema (due to the rupture of alveoli walls because
of the great air pressure at this level).
9.2.2. Specific signs
These signs are characteristic for each type of mechanical asphyxia and a re present to a
corpse together with the general signs (which may appear all or only some of them).
9.3. Types of violent death
9.3.1. Hanging
9.3.1.1. Definition : mechanical asphyxia due to the compression of the neck by a
traumatic loop acted by the weight of the body itself.
9.3.1.2. Classification – hanging may be:
Complete: when the whole body is hanging.
Incomplete: the body has a point of contact with the soil (the loop is acted by a
part of the body- for example the weight of the head is enough to pr oduce the
compression of the neck)
Also, hanging may be:
Typical: when the knot is in the back of the neck.
Atypical: when the knot is elsewhere (under the mandible, on the late ral part of the
neck, etc)
There are three types of loops:
Soft loops: for example muffler, tie;
Hard: for example wire;
Semi hard: for example cable, string.
9.3.1.3. Autopsy appearances:
External examination – the aspect of the hanging mark:
Localization – on the neck, mostly in the superior part (above the hyoid bone)
Direction – oblique, the upper point being at the knot.
Depth – the maximal depth is in the part opposite to the knot.
80
The hanging mark on the neck has the shape and the dimensions according to the
type of loop which was used.
The hanging mark is not completely circular because it is inter rupted at the knot
level. The dimensions of the knot mark are identical with the dimensions of the
knot.
Rapid dehydration of the hanging mark occurs; it becomes yellow-b rownish
colored (because the loop destroys the superficial layer of the skin).
Hanging mark is very resistant to putrefaction.
Sometimes, the forensic pathologist may find abrasion due to the nails, on the neck, around
and under the hanging mark (when the victim is desperately trying to remove the loop) and
also marks of other objects situated between the loop and the skin (f or example collar of a
shirt). There may be injuries on the body (bruises, abrasions, wounds) determined by
blowing the surrounding objects during the convulsions which precede death in hanging.
Post- mortal hypostasis occurs in the legs and hands if the body remains in vertical
position at least a few hours.
The internal examination may show:
Hemorrhagic infiltration of the muscle of the neck.
Fractures of both the hyoid bone and thyroid cartilage.
Damage of intima of the carotid arteries.
Fractures of the cervical spine, when hanging is performed with a chain (h ard loop)
or when the body falls very rapidly in gap (execution hangings).
In 90% of the cases hanging is the consequence of a suicidal act (used especially by
males). There are cases when hanging may occur as an acci dent (for example small
children that hang themselves with the swaddling band when they fall from bed) or a s a
murder (against persons which cannot defend themselves, drunken persons or per sons
with mental diseases). Also hanging may dissimulate a crime (suspending a corpse in a
loop). In these cases, we shall not find hemorrhagic infiltration in the muscle of the
neck and the forensic pathologist will observe lethal injuries with vi tal reactions,
produced by other methods (for example head trauma)
9.3.1.4. Death may occur in the following ways:
Compression of the superior respiratory ways;
Compression of the vessels of the neck; In these cases, the cya nosis and all the other
signs are obvious (“blue hanging”)
81
Death due to inhibition by stretching of the carotid sinus and causing reflex cardiac
arrest. In this case the classical signs of hanging are a bsent because death occurs very
rapidly (“white hanging”)
Spinal cord – brainstem disruption.
9.3.2. Strangulation
Definition: strangulation is the compression of the neck with a ligature or with the hand.
9.3.2.1. Strangulation with a ligature
A. Types of death
In almost all the cases (99%) is a murder, but it may be an ac cident (the case of Isadora
Duncan who died by strangulation with a scarf whose ends were fast ened round the
wheel of the automobile).
It may be also a suicidal act (a peculiar method used especia lly by the persons
suffering from mental diseases) known as the “turniquet method”, mea ning the
application of a ligature around the neck and twisting its ends on a wood or mental bar
fixed on the execution method in Spain in ancient times.
B. Autopsy appearances:
The ligature mark:
• may be seen on the neck, in its middle region;
• its position is horizontal;
• the ligature is complete, circular, without the mark of the knot as in hanging;
• the depth is equal on the hole circumference.
abrasion, bruises on the neck, around and under the ligature mark, due to the victim’s
fingers and nails;
general signs of asphyxia are intense (anoxia and vascular failure appe ar slowly)
internal findings: hemorrhagic infiltration in the soft tissues of the neck, fractures of
the hyoid bone.
9.3.2.2. Manual strangulation
9.3.2.2.1. Types of death
Manual strangulation is in 100% of the cases a criminal act, beca use a person is
able to press his own neck only until he losses consciousness and the musc ular
relaxation appears. Death is produced by anoxia or by a reflex mechanism
(compression of the carotid sinus with reflex cardiac arrest).
82
9.3.2.2.2. Autopsy features:
general signs of asphyxia (are absent when death is produced by a reflex
mechanism).
cyanosis is very intense, due to the slow compression of the neck;
the specific aspect is on the neck, where the marks of the fi ngers and nails of the
assaulter and of the victim are present. The finger pads produce discoi d bruises and
the nails produce semicircular abrasions. Usually, we may see on one late ral side of
the neck four discoid bruises, each having on its end a half moon abrasion, and on
the other side of the neck, a discoid bruise with a semicircular a brasion on its end
(specific aspect when strangulation is produced with a single hand).A ccording to
the position and the aspect of the marks, the forensic pathologist may establish the
way in which the strangulation was produced: using one or both hands, from t he
back or from the face of the victim, if the assaulter acts with the right or left ha nd.
at the internal examination, hemorrhagic infiltration in the musc les of the neck and
sometimes ruptures of the hyoid bone, may occur;
we may find also other signs of violence on the body, as a result of the fight
between the victim and the assaulter.
9.3.3. Suffocation
Definition: suffocation is a form of mechanical asphyxia due to t he blockage of the
nose and the mouth or of the upper airways with the impossibility of the air to enter the
lungs.
9.3.3.1. Suffocation by blockage of the external air passages (The nose and mouth)
Sometimes called “smothering”, it may be produced using the hand, soft fabrics, a
pillow or a plastic bag. There is a variety of suffocation call ed “gagging”, when
adhesive tape or fabric occludes the mouth to prevent speaking or shouting.
The mechanism of death is only the anoxic one
9.3.3.1.1. Types of death – t his form of suffocation may be:
a murder;
an accident: the suffocation of the baby with the mother’s hand when she sleep or
the suffocation of the epileptics falling with the face on a pillow or on soft soil,
during the access of epilepsy;
a suicide: very rare, with a plastic bag put on the head and face;
83
9.3.3.1.2. Autopsy appearances:
when the suffocation is produced with the hand, the forensic pathologist w ill find
bruises and abrasions on the cheeks, around the nose and mouth (due to the f inger pads
and nails);
when suffocation is produces with of a soft object (pillow) we do not find any injury
on the face. In this case it is very important to examine the internal side of the lips;
here we may find the prints of the teeth like hemorrhagic infiltr ation, due to the
pressure of the lips against the teeth (these signs are also present in suffoc ation with the
help of the hand);
when suffocation is produced with a plastic bag put on the head, the signs on the face
and also the signs on the internal face of the lips are absent;
the general signs of asphyxia are present.
9.3.3.2. Suffocation due to the blockage of the upper airways
The blockage of the upper airways may be produced with all kind of objec ts and
materials (for example soil, sand, vegetable materials, coins, food).
9.3.3.2.1. Types of death
Suffocation due to the blockage of the upper airways may be:
Accidental (the most frequent case). Example – children who introduce coins, bean
grains, little toys in the mouth, drunken persons, persons suffering fr om
neurological diseases (with swallowing troubles).
Crime: forcing an object in the mouth of the victim. In this case , injury of the lips,
teeth and tongue are present. Criminal infanticide may be produced by burring the
living baby (he inhales soil or sand).
Suicide: very rarely, in the past, inhalation of thin gold leaf was a common suicide
method (to disgraced mandarins).
9.3.3.2.2. Autopsy appearances
intense general signs of asphyxia;
injuries around the mouth and the nose;
injuries on other parts of the body due to the fight between the victim and the assaulter ;
opening the upper airways, the forensic pathologist will find the blocking object and
around and under it, the mucous have inflammatory signs (this is the proof that the
entrance of the object in the upper airways was during the life).
84
9.3.3.2.2. The mechanism of the death may be:
anoxia due to the blockage of the upper airways. If the upper airway s are blocked with
vegetable materials, the danger consists in the inhibition of these vege tables with
secretions from the airways, so their volume becomes larger and the blockage is
emphasized.
inhibition death- cardiac reflex arrest due to inhibitory reflexe s starting from the upper
airways mucous;
9.3.4. Thoraco-abdominal compression (“traumatic asphyxia”)
9.3.4.1. Definition
Thoraco-abdominal compression, also called traumatic asphyxia, is a mechanical
asphyxia produced by the compression of the thorax and abdomen, with hing ing the
respiratory movements.
Death is due to an anoxic mechanism. It appears in 30-40 minutes if the thorax is
compressed with 40-60 kg weight.
Characteristic: in the thoraco-abdominal compression, is the contras t between the
minimal lesions of the skin and the severe internal lesions.
9.3.4.2. Types of death
In most of the cases it occurs like an accident due to the land sli de ,catching the victim
under ruins in earthquakes, compressions of the baby with the mother’s ha nd during
her sleep (in some countries the law doesn’t permit the mother to sleep in the same bed
with a child under one years old).
It may be, also, a crime by pressing the victim’s body under the weight of the a ssaulter.
9.3.4.3. Autopsy appearances:
the general signs of anoxia are very intense (intense cyanosis , especially of the face,
intense stasis in organs, intense pulmonary edema with carmine a spect due to the
stagnation of the oxygenated blood in the lungs).
the skin have minimal injuries because of its elasticity;
at the internal examination we shall find multiple rib fractures , fractures of the
sternum, ruptures of the lung, heart and sometimes, of the organs of the upper
abdomen.
85
9.3.5. Drowning
9.3.5.1. Definition : is a form of mechanical asphyxia due to the replace of bre athed air
with a liquid in alveoli (water, wine, oil, etc.)
9.3.5.2. Mechanism of death in drowning
In sweet water death is due to ventricular fibrillation and cardia c insufficiency. The
sweet water is passing from the lungs in the blood vessels (due t o the increased
osmotic pressure in the vessels and the small pressure in the lungs ) so, the dilution of
the blood occurs with the growth of the circulatory blood volume.
In salted water death is due to anoxia determined by the concentrati on of the blood and
the pulmonary edema. In this case, the liquids from the vessels a re passing in the lung
from a small to a bigger osmotic pressure and the pulmonary edema occurs.
Glottis reflex and death by inhibition due to the entrance of the water in the lary nx.
Allergic mechanism due to the contact between the skin and the cold water; in thi s case
death occurs without any signs of anoxia.
9.3.5.3. Clinical aspects in drowning:
The drowning is produced in four stages:
• Reflex apnea (1 minute): for hinder the aspiration of water.
• Expiratory dyspnoea, as a protection mechanism against the water entering in
the lungs (1-2 minutes);
• Convulsions: due to cerebral anoxia.
• Respiratory break followed by ample respirations. In this stage, a great quantity
of water is inhaled and swallowed. After this stage, death occurs.
Death in drowning occurs in 3-10 minutes. It may occur more rapi dly in cases of
glottis reflex or allergic mechanisms .
9.3.5.4. Autopsy appearances:
Signs of immersion:
• these are lesions due to water;
• these signs appear on each body who stays in water, no matter t he cause of
death;
• they may help to appreciate the period of time in which the body was
immersed;
• a peculiar sign is the “goose flesh” due to contraction of the erect or pilae
muscles (attached to each hair follicles) at the contact with the cold wat er.
86
Maceration of the skin:
• appears first at the hand and feet, depending on the period of time in w hich
the body was immersed;
• the skin becomes white on the palms and plants in 3-6 hours;
• in 3-5 days the “laundress grove” appears (the wrinkling of the skin f rom
the finger pads);
• the skin of the hands and feet becomes detached in 10-15 days;
• the detachment of the “death grove” after 1 month;
• the hair becomes to fall in 10 days;
• deposition of mud, oil, silt, cool-slurry on the body and even in the hair,
mouth and nostrils;
Lesions due to the animals:
• the aquatic animals may destroy parts of the corpse (detachment of fingers,
of the nose, ears and so on). Characteristic for these lesions is the absence
of the hemorrhagic infiltration (indicating the lesion are produced af ter
death);
Lesions due to the blow with stones, bridges, propellers of the ship:
• these injuries may be serious, like fragmentation of the body by t he
propeller of a ship;
• we may also find injuries due to dragging of the body on the bottom of t he
water (especially in running waters);
• we may also find injuries due to jumping in the water- injuries of the spine,
organs (due to the contact with the surface of the water)
Drowning lesions:
• Due to the entrance of the water or other liquid in the organism, i n this way
they constitute a proof of the vital nature of drowning;
• fluid blood in the left heart and, sometimes, liquid in the pleural cavi ties
(due to resorption of the breathed water)
• the “drowned man mushroom”- is a white foam around the mouth and
nostrils, due to the mixture between the breathed water, air and mucus from
the lungs;
87
• the lungs are over inflated, filling the thorax and covering the hea rt. The
elasticity is diminished and on the section has a drying aspect – acute
pulmonary emphysema due to the rupture of the alveoli walls;
• Paltauf spots – on the serossa, especially on the pleura. They are bigger than
Tardieu spots, have the same producing mechanism and blue color;
• water in the stomach and intestines;
• soils mug, algae in the respiratory ways;
Signs of anoxia:
• the general signs of asphyxia;
Putrefaction aspects: are characteristic in drowning.
• the putrefaction in water begins from the head (“black head”) and, a fter this
goes downward to the thorax;
• if the body stays in water more than 2-3 months, the formation of soaps
begins on the corpse;
9.4. Laboratory examinations
Examination of diatoms: The diatoms are microscopic algae with a silicaceous
exoskeleton. The type of diatoms varies in different waters and that is why the
examination of diatoms shows if the person drowned in the same wate r where the body
was found (in murders, the person may drown in a water and after deat h the body is
moved to another water).
The test also indicates if the drowning was vital (the victim was alive at the drowning
moment). If the forensic pathologist distinguishes diatoms in the orga ns with terminal
circulation (bone narrow, spleen, kidneys) that means that drowning was vital;
9.5. From juridical point of view
9.5.1. Accident
the most frequent;
The following elements are pleading for an accident:
• high level of alcohol in the blood;
• drowning in small waters (the drunken person may fall with the face down
in a water puddle and drown. It is enough the mouth and nostrils to be
under water for the drowning to occurs).
88
9.5.2. Suicide:
other suicide attempts in the past, even by other methods than drowning;
old persons, without other injuries;
explanatory letters addressed to the family and friends;
evidences of mental diseases ;
9.5.3. Crime:
on the corpse we may find also other types of injuries (like ligature marks on the
neck).
the hands and feet may be tied;
a gag in the mouth;
a heavy object attached to the body;
on the body we may find marks of a fighting;
89
CHAPTER 10: DEATH CAUSED BY ENVIRONMENTAL FACTORS
10.1. General aspects
We have four types of death caused by environmental factors:
1. Hypothermia
2. Hyperthermia
3. Burns and scalds
4. Electrical fatalities
This types of death have two types of injuries: thermal injuries and electric injuries.
10.2. Thermal injuries
10.2.1. Low temperatures injuries
10.2.1.1. Hypothermia
Definition : indicates the cooling of the human body below 35 degrees C, which appear s
when loss of body heat exceeds heat production.
We have two types of hypothermia:
• dry cold hypothermia;
• immersion hypothermia.
Factors involved in hypothermia:
Low environmental temperature: air temperatures below 10ș C may c ause
hypothermia in vulnerable person;
Humans are able to retain body heat balance in water at 22șC. Under this level, loss
of heat gradually occurs and below 16 șC, survival time decreases sharply;
Immersion hypothermia is more grave due to the more rapid loss of heat in water
than in air (three times faster);
Because of the thicker layer of subcutaneous fat, women tolerate c old water better
than men do;
Infants are unable to regulate body temperature and thus can be af fected by
hypothermia even in a tropical climate. The most dangerous period is i n the first
two weeks of life;
Young adults are affected by low ambient temperature under conditions of physical
exhaustion and influence of alcohol or drugs;
90
Elderly are affected by a combination of debilitating disease s, impaired ability to
maintain body temperature and inadequate nutrition.
Pathophysiological effects of cold
The critical ambient air temperature is 27 degrees C, when it is possible to retain constant
body temperature in the absence of physical activity. The damages occur in a ll systems.
Nervous system :
A body temperature of:
• 32 degrees C:analgesia, clouding of consciousness, hallucinations, slowi ng of
reflexes;
• 30 degrees C: cold narcosis;
• 27 degrees C: reflexes are abolished;
• 26 degrees C: pupilar reaction disappears, the victim fails to underst and when
spoken to.
From this body temperature, permanent brain lesions like epilepsy a nd dysphasia may
occur because of the severe diminished blood flow. Conduction velocity in pe ripheral
nerves decreases with the lowering of the nerve temperature and pa ralysis of peripheral
nerves, occurs at about 20 degrees C.
Heart and circulatory system
decrease in pulse rate is linear with the lowering of body temp erature, except for
spasmodic elevations associated with shivering.
EKG :
• prolongation of the P – QRS wave;
• inverted T waves;
• “I – wave” appears after the P – QRS complex (around 30 degrees C body
temperature).
• below 30 degrees C – atria fibrillation;
• at 25- 28 degrees C – ventricular fibrillation;
• below 20 degrees C – if the heart escapes fibrillation, it beats very slowly (at 11
degrees C a woman had 4 beats/ minute). After rewarding, the norma l rhythm was
reestablished;
• at 10,5 degrees C – the heart stops.
91
Blood pressure :
• during the first excitation phase of hypothermia (37 – 34 degrees C) the blood
pressure becomes elevated, but afterwards it decreases;
• at 25 degrees C – about 30 mm of mercury;
• usually under 25 degrees C, blood pressure is undetected.
Respiratory system
respiratory regulation seems to remain effective even at 25 degr ees C although
respiratory rhythm can be reduced to a few excursions per minute;
cold may cause mild lesions in the bronchiolar and alveolar epithelium that open the
way to bacterial invasion. This is the cause of the frequent occur rence of respiratory
complications following exposure to environmental cold.
Gastrointestinal tract
paralysis of the intestines is the cause of the abdominal pains of the victims re scued
from cold exposure;
hemorrhages and erosions of the gastric mucous, called , called “Vischnevski ulcers”;
ulcers of the same nature may be found in the ileum and colon.
Blood
hemoconcentration because of cold diuresis and leaking of plasma into the
extracellular spaces (“cold edema “);
high hematocrit values because of hemoconcentration;
dissociation curve of hemoglobin is shifted to the left, causing a tighter binding
between oxygen and red blood cells ->oxygen is not available to the tis sues ->systemic
anoxia. This is partly compensated for by acidosis (the blood pH can be lowered to 7,2)
hyperglycemia occurs in the early phase of hypothermia;
decrease in the number of blood eosinophils;
elevation of the serum potassium level, and decrease of the sodium.
Surviving time in cold
Results of the experiments in Dachau, Second World War:
one hour is necessary for a man to die immersed in water at 4 degrees C;
in northern Atlantic, water is about 0 degrees C in winter. Fatal c ooling occur in half
an hour;
swimming in cold water increases heat loss owing to blood flow to the body surface;
92
in water over 20 degrees C, a man can swim indefinitely without manifestations of
hypothermia;
surviving time in dry cold is much longer than in cold water. Fact ors like wind
velocity, humidity of the air, determine big change in the surviving time.
other factors:
• age of the person;
• health state;
• thin or fat;
• influence of drugs and alcohol;
• protected by clothes;
Autopsy findings:
A. External examination
reddish – pink discoloration of the skin(cherry red lividity).
• usually seen at the hands, elbows, knees and feet;
• sometimes the body is white (“white death”);
• blue spots on the hands, knees, feet, which probably represent frostbite.
• Mechanism: red color of the skin is due to ante-death binding of oxy gen to
hemoglobin and its post-death diffusion through the skin.
• Histological: edema and hyperemia of the dermis with occasi onal foci of
inflammatory cell infiltration.
Edema:
• specially at the legs;
• may precede hypothermia because of a chronic heart failure of the victim;
Blisters: because of the edema which accumulates under the skin.
B. Internal examination
Acute gastric erosions – Vi șnevski erosions: hemorrhages and erosions in the gastric
mucous in the deep of which we may find coagulated blood of brownish color; the re
are found more often in old people.
Acute pancreatitis: not accepted by all the authors; found also bef ore death;
ATTENTION: not to be confounded with pancreatic putrefaction.
Hemorrhages into the pancreas: appears sometimes.
Acute heart failure:
– dilatation of the right atrium and ventricle;
93
– congestion of the vena cava;
frothy bloody fluid in trachea and bronchi;
Edema, congestion and hemorrhage in the lungs;
Congestion of liver and spleen;
Bronchopneumonia: frequent complication that develops in 50% of the cases of
survives.
Kidneys: acute tubular necrosis; lipid deposition in glomerule; meas uring the
cathecolamines in the urine is important, they are often found in ample amounts in
victims of hypothermia.
Brain edema.
Perivascular hemorrhages: are located especially in the bra in in the walls of the
third ventricle (not specific for the hypothermia).
CONCLUSION: because specifically signs are not found, we may consider that a body
with very well preserved tissues at histological examination, m ay be suspected of
hypothermia because of the delayed putrefaction due to the low tempera ture where it was
exposed.
TO NOTE :
• physical exhaustion and alcohol or drugs are frequently contributing factors;
• exercise leads to rapid exhaustion because muscular activity inc reases the demand
for oxygen and head production;
• perspiration produced by exercise reduces the insulation of clothing;
• insufficient nutrition can be a precipitating factor.
• the victim of hypothermia may be found undressed because of:
-hallucinations;
-a felling of warmth due to paralysis of thermoregulatory mechanisms;
-the effects of drugs and alcohol;
-a large output of epinephrine;
The type of death by juridical point of view
Accidental: very often.
Suicide: rare, in psychiatric diseases and alcohol consumption;
Crime: especially children or persons with handicaps;
Dissimulation of a crime: by hypothermal death is not advisable be cause cold
preserves very well the marks of violence on the body;
94
Work accident: rare, in industry;
Medical malpractice: rare, in industry.
10.2.1.2. Local injury due to cold. Frostbite
A. Immersion foot and trench foot
Occurs commonly when temperature is between 5-8 șC;
Contributor factor: wetness;
Obliterating angeitis causes severe gangrene and lost of tissue.
B. Frostbite:
occurs on exposure to dry cold as well as following immersion at temperatures below
0șC, usually above – 2,5 șC.
frostbite degrees:
• First degree: redness and edema of the skin; the lesion heals prom ptly without
permanent damage;
• Second degree: epidermis is affected and there is blister forma tion but the
underlying tissue are not involved;
• Third degree: skin and subcutaneous tissue are necrosis;
• Fourth degree: total loss of tissue in the exposed area, including muscle and
eventually bone;
moderate concentrations of alcohol (0,06-0,15 per cent in blood) may have a pr otective
effect against frostbite.
It is commonly seen in mountaineering and polar expeditions.
10.2.2. High temperatures injuries
There are two types of lesions produced by high temperatures :
Hyperthermia;
Burns and scalds.
10.2.2.1. Hiperthermia
• An elevated core body temperature of 40.5 șC or higher;
• All hyperthermic death is accidental.
Forms of heat illness:
• Heat cramps;
• Heat exhaustion;
• Heat stroke (risk factors: alcoholism, atherosclerosis, obesity).
95
Autopsy finding of hyperthermic deaths :
• Are nonspecific;
• Visceral hemorrhages and congestion of the heart, lungs and kidneys;
• Victims who survives form more than 24 hours show lobar pneumonia, acute
tubular necrosis, centrilobular necrosis, adrenal necrosis and hemorrhages;
• Heart shows subendocardial hemorrhages, changes in the muscle fibers;
• Cerebral edema.
10.2.2.2. Burns and scalds
Survival following burn injuries depend on:
• The severity and extend of the burn;
• The age of the victim: in children, burns over 20% body surface are da ngerous
for life; in adults, burns over 40% are dangerous;
Classification of burns:
• First degree burns.
o damage is limited to the outer layer of the skin;
o blisters do not form;
o the burned area is red due to congestion, swollen due to edema and painful;
o on a dead body discoloration rapidly faded, so it may not be recognizable;
o mild sunburns may be classified like first-degree burns;
• Second degree burns.
o appearance of blisters;
o upper layers of the skin are destroyed;
o scarring sometimes follows;
• Third degree burns.
o involves the entire thickness of the skin;
o epidermis and dermis are damaged;
o pain is absent because nerve endings in the skin are destroyed;
o scarring is the rule;
• Fourth degree burns (charring).
o complete destruction of the skin and underlying tissues.
Classification of the severity of burns:
“Wallace´s rule of nine” is a way of estimating medium to large burns in adults, body is
divided into areas of 9%:
96
• head=9%
• each upper limb=9%
• trunk=36%
• each lower limb=18%
• genital external organs=1%
Severity of burns depends on:
• the intensity of the heat
• duration of exposure.
TO NOTE:
• clothes contribute to faster destruction: however, tight clothing (belt s, shoes)
preserve underlying skin from burning;
• rib cage, facial skeleton and arm bones are exposed after 20 minutes of a normal
house fire; leg bones are exposed in about 35 minutes;
• using of a flammable liquid, results in patchy charring of disproportionate se verity;
• every piece of glass at a fire scene may indicate whether the glass was broken
before or after the fire started;
• characteristically curved fractures are seen only in bones e xposed to high
temperatures. These cracks occur when the bone is allowed to cool aft er removal
from the fire. Continued exposure to intense heat causes bones to break up into
paper-thin sheets of calcium matters.
• a fire in the open does not usually permit complete combustion of a body.
• teeth, like bones, are resistant to fire, giving an excellent means of identif ication.
• the rate of decomposition of a severely burned body is considerably delayed.
Examination of a burned body
Objectives:
• identification of the victims;
• determining the cause of death;
Identification of the victims
weight and length of a charred body are unreliable;
the features are changed by skin shrinkage;
identifiable peculiarities (scars, tattoo) are destroyed;
97
distinction between the sexes can be made by examination of inte rnal genital organs
and breasts;
racial identification is possible with the help of patches of intact skin
unburned skin in some area of the body suggests compression of some mate rial on this
area;
hair changes color on exposure to heat depending on the temperature. Bla ck hair
doesn’t change color.
X-ray examination may find old fractures, bones abnormalities or f oreign bodies. X-
ray examination of teeth may reveal metal treatments.
in the hands, the skin comes off like a glove, including the fingerna ils. This may be
used to obtain fingerprints.
Determining the cause of death
first, we must establish if the victim was alive at the time of the fire. Ev en low levels of
carbon monoxide in the blood are significant;
a “mushroom” of thick, white foam at the nostrils or mouth indicates that the victim
was breathing while the fire was in progress;
absence of carbon monoxide in the blood does not imply that death has occurred before
the fire. The cause of death may be a flash fire or an explosi on, when death is
instantaneous. Inhalation of superheated air, causes edema of the a irway and rapid
death as a result of suffocation;
three-quarters of all fire-related deaths result from inha lation of toxic smoke (synthetic
objects, plastics). In addition to large amounts of carbon monoxide, burning polymers
produce hydrogen cyanide. The human lethal level of blood cyanide is 5 mg/m l.
Carbon monoxide interferes with the ability of blood to carry oxygen and hydrogen
cyanide interferes with the ability of cells to utilize oxygen;
COHb levels of over 10% in a burned body indicate that smoke inhalations oc curred.
Sometimes, a few breaths of such smoke are enough to reach this level;
inhaled smoke is seeable in the nostrils and mouth, and may remain for days in victims
who survived. Small flakes may be recovered from the esophagus and stomach;
blisters in the skin do not necessarily indicate that the victim was alive at the time of
fire;
the body assumes a position often referred to as pugilistic; inter esting, this position
develops during the cooling process, following the fire;
98
artifact fractures of the skull caused by heat are seen in bodies recovered from fire;
they consist of several lines radiating from a common center; the edges of a heat
fracture are usually more irregular and ragged than those of a physical trauma ;
heat fractures do not generally involve the sutures of the skull;
presence of blood under the dura mater always indicates an injury sus tained while the
victim was alive and is not related to the effect of heat;
the presence of alcohol in a subdural hematoma may be possible after four days from a
fatal head injury;
splits due to heat involving the abdominal wall, invariably run parallel to the muscle
fibers. Any split across a muscle is the result of physical trauma;
fire victim’s anus is occasionally dilated and sometimes the re ctal wall protrudes
through the opening. This could be mistaken for evidence of sexual perversion.
10.2.3. Injuries due to scalding
Depends on:
• the temperature of the liquid;
• duration of the contact;
• sensitivity of the skin; the mucous membranes of the mouth and throat are more
resistant to hot liquids as skin;
• certain areas of the body are more sensitive than others (the pal m surface is more
resistant than the face, abdomen or genital organs);
• household hot water may produce severe burns at 2-3 seconds of exposure;
• clothes worsen the damage by prolonging contact with the hot liquid by reducing
the cooling effect of evaporation;
• the disposition of scalds on the body may show if the scalding was a ccidental or
criminal; this happen especially in children;
10.3. Electrical fatalities
10.3.1. General aspects. Definition.
Definition : the body is incorporated into an electrical circuit, so there ar e a passage of
electrons though the tissues, producing a biological damage. The cu rrent enters at one
point and then leaves the body at an exit point, usually to the eart h. The gravity of the
lesions depend on the vital structures which happen to be in the way of the current.
99
Fatal electrocution may occur in three major events :
• Passage of current across the heart usually from a hand to the earthed feet. C ardiac
dysrythmia occurs, usually a ventricular fibrillation ending in asystola;
• Passage of current across the chest and abdomen, lead to respiratory paralysi s from
spasm of the intercostals muscles and diaphragm;
• When the current passes through the head, it has a direct effect on the cardiac and
respiratory centers, which are paralysed.
10.3.2. Electrical considerations
We must consider the next terms:
• The Law of Ohm.
• Alternating and direct current.
• Current.
• Voltage
• Resistance
• Law of Ohm: Current= Voltage/Resistance
Alternating and direct current
• direct current is less dangerous than alternating current (for example: 50- 80
mA alternating current is fatal in seconds whereas 250 mA dire ct current is
often survived);
• alternating current is four to six times as likely to cause death because of
the “hold-on” effect, result of tetanus muscle spasms which prevent s the
victim from releasing the conductor;
• alternating current between 40 and 150 cps produce more often ventri cular
fibrillation, the usual house frequency being of 50 cps. Over this li mit,
fibrillation is more rare.
Current: The degree of damage to the tissues is proportional to t he quantity of
electricity flowing through them.
• Values: 30 mA = painful muscular contractions
40 mA= lost of consciousness
50-80 mA= risk of death
Voltage:
• most of the fatalities occurs with the domestic voltage of 220 V;
100
• time of exposure has a very important role, even smaller voltages being able
to produce death if they action for a long time;
• extremely high voltages are safer, as the shock may fling the s ubject off the
conductor.
Resistance:
• the major barrier is the skin which has a far higher resistance than organ.
That is why skin electric burns occur. The resistance of the skin varies
according to the thickness of the keratin- covered epidermis.
• average resistance of the skin is 500-10000 Ohms.
• dryness or wetness of the skin, greatly affects its resist ance. Dry palm skin
may have the resistance of 1 MOhms, when wetter this may fall to only 1200
Ohms.
10.3.3. Effects on muscles
spasm of skeletal muscles, especially the stronger flexor mus cles of the arm=>”hold-
on” effect. This increases the time of contact and the risk of c utaneous burns or cardiac
or respiratory arrest.
“hold-on” effect appears at 9-10 mA.
10.3.4. Mode of death
Ventricular fibrillation: caused by the passage of current through the myocardium,
disturbing the conducting system. The body is pale and the autopsy is “white”
except possible electrical marks.
Respiratory arrest: by spasm of intercostals muscles and dia phragm. The body is
congestive.
Delay between shock and death: rather often, the victim is able to recover or to
move on small distances. Persons are found dead later, many elect rical deaths
being not observed, so the autopsy is difficult.
The non-electrical trauma: because of the shock, the victim may fa ll from a height
suffering severe head trauma.
10.3.5. The cutaneous electric mark
It may be present or absent depending on:
• The skin area (electrocution in the bath leaves no signs);
• The conductivity.
101
The coetaneous electric mark represents the thermal burn from heating of the epidermis
and dermis as the current passes. The lesion is more severe as the surface of contact is
smaller. The mark is not a simple burn, there are nine features how ever which are
characteristic of an electrical cause:
Firm contact->tissue fluids are heated up->steam->this may spl it to layers of the
epidermis->raised blister which collapses->annular, with a raise d gray or white
ring and an umbilicated center.
Less firm contact->the current jumps the gap as a spark->hard brow nish nodule
raised above the surrounding surface, called “spark” lesion.
When the time has been prolonged ->severe burn, with large areas of peeled
blistered skin, charred keratin and a mixture of hyperemia, deep scorching and she d
epidermis.
Commonest feature: an areola of blanched skin at the periphery.
High-voltage burns->multiple spark lesions, giving rise to a “crocodil e-skin”
effect.
“Earthling lesions”-similar but less severe. Should be looked for on t he other hand
or on the feet.
In exposure for a long time->effects as in high voltage burns, c harring and more
extensive peeling and blistering of skin with deep muscle damage a nd cooking of
the tissues. Much of this damage may occur post-mortem.
Sometimes marks may keep the form of the object in contact.
A contact with a metal conductor produces metallic ions to penetrat e the skin and
even the subcutaneous tissues. These may be invisible to the eye, but de tectable by
chemical techniques.
10.3.6. Internal appearances
internal tissues are largely aqueous and contain conductive electrol ytes, which marks
the current to be to diffuse to cause thermal damage.
the body is pale in ventricular fibrillation or with marked congest ion and cyanosis of
the face with similar changes in the lungs, in spasm of the diaphr agm. Dark blue red
post-mortem hypostasis is the sign of a congestive death.
102
10.3.7. Histological appearances
Controversial : some changes considered like electrical lesions, have been shown t o be
thermal.
vacuolations of the epidermis and sometimes dermis;
the cap of the epidermis may be detached and raised into a blister;
histochemical reactions for metallization;
the cells of the epidermis are elongated with the nuclei orientated and stret ched;
scanning electron microscopy is the best way of distinguishing betw een electrical and
thermal damage; wavy appearance of the myocardial fibers and their fragm entation.
10.3.8. Particular cases
10.3.8.1. Electrocution in the bathroom
The bathroom is a common site for electrical tragedies, due to:
• moist atmosphere;
• ample water;
• good earthling through metal pipes;
• wet, unclothed body.
Unusual demarcation of post-mortem hypostasis in such deaths, where the water le vel
during electrocution appears to limit the subsequent appearance of the hypostasis.
10.3.8.2. Death from lighting
lighting deaths are only accidental, but the nature of death may be unc ertain if a dead
body is discovered in the open with no marks upon it;
helpful aspects:
• reports of lightning strike nearby;
• torn and scorched clothes;
• magnetized metallic objects in the pockets;
• smell of burning about the body and clothing;
lesions are very unpredictable, going from mutilation to unharmed;
cutaneous marks may be present as the well-known “arboresque” patte rn like irregular
red marks, often linear first degree burns.
103
CHAPTER 11: THE DEATH DUE TO CHEMICAL AGENTS –
INTOXICATIONS
11.1. General aspects
11.1.1. Definition : the toxic is any substance which, introduced in the organism, may
produce a pathological state named “intoxication”.
11.1.2. Classification of the toxic substances: there are multiple classifications of the
toxics. Some of them are:
• According to the origin of the toxic:
• Vegetable.
• Animal.
• Mineral.
• According to the aggregation state of the toxic:
• Gaseous.
• Solid.
• Liquid.
• According to the anatomo-pathological lesions due to the toxic:
• Toxic substances which produce injuries at the entrance gate (like acids,
alkali).
• Toxic substances which produce general injuries after their absorption.
• Toxic substances which produce minimal and uncharacteristic lesions ,
like functional toxics.
• By clinical point of view, the intoxications may be:
• Acute.
• Subacute.
• Over acute.
• Chronic.
11.1.3. By juridical point of view, the poisonings may be:
• accident;
• suicide – a form of passive suicide is the drug addiction;
• crime.
104
• The minimal lethal dose is the minimal quantity of toxic substance which
may produce the death to an adult person. For the children, the minimal
lethal dose is smaller than that of the adult, and may be calculat ed according
to Young’s formula:
V/V plus 12, where V= the age of the child (in years);
For example: for a child of six years old, the minimal lethal dos e is: 6/6 plus 12=1/3 from
the adult’s minimal lethal dose;
11.1.4. The toxicity of a substance depends on:
External factors:
• the way and the rhythm of entrance of the toxic substance (for example on
respiratory way and by injection, the toxic substance enters more rapidly in
the organism);
• the concentration of the toxic substance –the toxicity is proportional w ith
the concentration;
• the physical and chemical properties of the toxic substance and a lso added
substances (may change the absorption, the metabolism or the eliminat ion
of the toxic substance).
Internal factors:
• the age – the toxic substances are more dangerous for the children a nd for
the old persons;
• pathological states which diminish the organism’s resistance aga inst the
toxic substance;
• the sex – the women are more sensible;
• sometimes, the race.
11.2. Types of intoxications
11.2.1. The Ethyl Alcohol Intoxication
Ethyl alcohol is the most commonly used drug in the world.
11.2.1.1. Entrance ways:
• orally (by ingestion) is the most common way;
• inhalation – very rarely.
11.2.1.2. Absorption:
105
The ethyl alcohol is rapidly absorbed through all the mucosa, start ing from the mouth,
but the faster absorption is in the first part of the small intestine (especial ly duodenum).
The speed of absorption depends on:
concentration of the drink – very strong drinks (over 40% alcohol) slow the rate of
absorption because of the pyloric spasm, irritation of the gastric lining (forming a
barrier of mucus), reduced gastric motility;
the rhythm of ingestion;
the absence or presence of the food in the stomach:
• in a full stomach, the absorption is diminished;
• in an empty stomach, the absorption of the alcohol occurs in 30-60 minutes;
in a full stomach the absorption is delayed until two hours;
• a fatty meal, the milk, slow the absorption even more;
some drugs may affect the absorption rate by modifying the speed of stomach
emptying;
diseases of the stomach.
11.2.1.3. The metabolism:
Almost all alcohol is metabolized by the liver; between 90-98% of i ngested alcohol is
removed from the blood by the liver, only 2-10% being excreted unchanged.
There are three metabolism ways:
The alcohol dehydrogenises way: the alcohol metabolism is due, in the first stage, t o
its oxidation in acetaldehyde, performed by an enzyme named” alc ohol
dehydrogenises”; the second stage consists of acetic acid form ation, performed by
acetaldehyde dehydrogenises (it is more rapid than the first stage, that is why
acetaldehyde cannot be accumulated in the organism); the acetic acid is rapidly
oxidized further to carbon dioxide and water.
The microsomial system way (MEOS) – is involved only in big inge stion of alcohol
or in repeated ingestions.
The catalyses way (cat).
These last two ways are rarely involved in alcohol metabolism, the alcohol
dehydrogenises way being the most important.
The speed of detoxification in the liver is constant and it has be en assumed that blood
alcohol declines at a rate round 15 mg%0/hour.
106
In some of the oriental people there is an immediate hypersensiti vity to alcohol
ingestion, named “oriental reaction” or “flash reaction”, due to acet aldehyde
accumulation because of the alcohol dehydrogenises increasing or a cetaldehyde
dehydrogenises diminution. This is a state due to the hallucinogen ef fect of
acetaldehyde, but is different from the pathological drunkenness.
11.2.1.4. Elimination of alcohol:
2- 10% of the ingested alcohol is eliminated unchanged by the kidneys, lung s, sweat,
salivary and mammary glands;
the main ways of the metabolized alcohol elimination are the kidneys and the lungs;
the urine contains a bigger quantity of alcohol than the blood, the report bet ween them
being: urine concentration/ blood concentration= 1,30- 1,40;
the expired air may be used also for the alcohol’s blood level estimation: 1ml. Of blood
contains the same quantity of alcohol as 2,1 l. of alveolar air.
The metabolism of alcohol may be represented by the Widmark’s curve: the upward
part represents the absorption; then, there is a small plateau re presenting the short
period between the absorption and elimination; the last part is downw ard one,
representing the elimination phase.
11.2.1.5. Mode of action of alcohol:
The ethylic alcohol has a depressant action on the nervous system. E thyl alcohol
determines a state of hypoxia to the neural cells, reducing their activity .
The depressant action begins in the superior parts of the brain (the most developed),
and goes down through the bulb. If only the superior parts of the brain are affected, the
behavior will be more primitive and unrestrained, which seems to be a false simulator
effect (the inferior parts of the brain being uncontrolled by th e superior parts due to
their inhibition).
11.2.1.6. The symptoms of acute alcohol intoxication:
The first symptoms appear, to accustomed people, to a blood level around 0,20 – 0,40
g%0.
The first phase (until an amount of 1g%0 alcohol in the blood):
• expansively grows, the person speaks fast and a lot, the behavior is
unrestrained, uncontrolled;
• a false impression of increased cerebral activity; actually , the acoustic
and visual perception, the speed of the reflexes are diminished;
107
• neurovegetative symptoms: perspiration, the sensation of warmth (due
to dilatation of the peripheral blood vessels).
The second phase (alcohol level between 1- 2,50 g%0):
• the troubles from the first phase increase;
• confusion, disconcertion, the judgment and the memory affected;
• neuromuscular troubles: balance troubles, ataxia, troubles of the speec h,
increased heart and respiratory rhythm, hiccup, vomits, intense
congestion of the face;
• excitement state, sometimes;
• In that phase, named the medico-legal phase, the biggest part of the
felonies occurs (aggressive acts with strikes, murders, accident s, thefts,
burglaries).
The third stage (the alcohol’s blood level between 2,5 – 5g%0):
• profound sleep;
• anesthesia;
• hypothermia;
• The evolution may be through coma with the disappearance of the
reflexes, dilatation of the pupils, small arterial pressure.
• The death may occur by the paralysis of the respiratory bulbar center.
• The minimal lethal dose in alcohol intoxication is around 3,5 – 4.5g/kg
weight.
11.2.2. The Alcohol Intoxication (Other Than Ethanol)
11.2.2.1. ETYLENE GLYCOL
Source of exposure:
Approximately 85% of all ethylene glycol produced is used either a s an
antifreeze or in the production of polyester. Antifreeze mixtures contain up to
95% ethylene glycol.
Many cases of ethylene glycol poisoning results from accide ntal ingestion by
children who can take in large amounts since the substance tastes good.
Alcoholics may also ingest this substance as an ethanol substitute.
Absorption: oral ingestion.
Distribution: the two primary distribution sites where metabolism to toxic me tabolites
occurs, are the liver and kidney.
108
Metabolism:
The toxicity of ethylene glycol itself has been found to be low, it is metaboli zed
to toxic metabolites: glycolaldehyde, glycolic and glycoxalic acid and oxalic
acid.
Oxidation of ethylene glycol occurs in the liver and kidney, yielding
glycoaldehyde. Glycoaldehyde is further oxidized to glycolic acid. Oxalic acid
is produced from further oxidation of glyoxylic acid. Glyoxylic aci d can also
induce formation of lactic acid.
The major toxic metabolite of ethylene glycol appears to be glycolic a cid.
Elimination:
oxalic acid as an end product chelates calcium ions forming insoluble calcium
oxalate monohydrate crystals that can be eliminated in the urine.
Half-life in the serum is approximately is 2 – 3 hours.
Critical sites of toxicity:
• Heart, central nervous system, respiratory system and kidney;
• Ingestion of as little as 150 ml of ethylene glycol has been show n to be
fatal.
Clinical manifestation: there are three stages of ethylene glycol toxicity in huma ns,
all of which have found to occur within a 72 hour period post-ingestion:
The first stage involves metabolic changes, gastrointestinal upse t, and central
nervous system depression, and spans the period of 30 minutes to 12 hours
post-exposure.
The second stage occurs between 12 – 24 hours post-exposure, is charact erized
by severe serum hyperosmolarity and cardiac symptoms (tachypne a,
hyperpnea, and tachycardia), all of which are primarily due to met abolic
acidosis. Glycolic acid and lactic acid are the contributors to t he production of
metabolic acidosis.
The third stage of toxicity, which is evident approximately 24 – 72 hour s post-
exposure, involves adverse renal effects, including flank pain and polyuria.
Recently, a fourth stage has been proposed, occurring 6 – 13 days post-
exposure, called the late cerebral stage.
Treatment : sodium bicarbonate, hemodialysis.
109
Autopsy appearances:
There are no characteristic autopsy appearances;
The forensic pathologist may see:
• generalized congestion;
• stasis in the internal organs;
• cerebral edema.
11.2.2.2. METHANOL
Is a clear, colorless, volatile liquid with a weak odor.
Products that contain methanol: windshield wiper fluids and de-ices, anti freeze, glass
cleaner, canned heat, paints, varnishes, paint thinners and removers.
Absorption:
through gastrointestinal tract mucous, skin and lungs.
Distribution: rapidly distributed in the body water with peak blood level s
occurring in about 30 to 90 minutes after exposure.
Metabolism: methanol is metabolized by alcohol dehydrogenises to formaldehyd e and
then to formic acid. It is these two metabolites that cause toxi city with formic acid.
Formic acid causes the profound metabolic acidosis and blindness.
Clinical manifestation: the first 1 – 2hours may be similar to ethanol intoxication in
that the patient may have drowsiness, vertigo and uninhibited behavior. Vi sual
disturbances are the classic symptoms, include decreased or blurr ed vision. Coma,
seizures, blindness. Death caused by renal failure, cardiac fail ure and pulmonary
edema.
Treatment: gastric lavage to remove any residual gastric methanol; e thanol is used to
decrease the metabolic degradation of the methanol to its toxic metabolites ; dialysis.
11.2.3. Carbon Monoxide Intoxication
The carbon monoxide is formed by the incomplete burning of carbon or of the
substances with rich carbon contain.
11.2.3.1. Sources of carbon monoxide:
in the atmosphere of the big cities there is carbon monoxide betwe en 1/100.000-
1/10.000; at that last concentration, its presence begins to be felt;
domestic heating appliances in bad repair may produce CO when incomplet e
combustion of the fuel takes place;
110
the engines of the motor vehicle emit up to 5-7% CO in their exhaust fumes; and more
if the engine is defective or improperly tuned. When the exhaust fumes are confined to
a small place, a dangerous or even lethal level may be reached in short time .
a suicide method is sitting in the garaged car with a window open and allow the gas to
enter in the car; another method is using some device which permit t o pipe the gas into
the interior of the car and this way may be done outside a garage.
fires in buildings; it was estimated that the majority of dea th in house conflagrations
are caused not by burns, but by inhalation of the smoke containing big amounts of CO.
carbon monoxide may be the result of many industrial processes, espec ially in iron and
steel workers;
carbon monoxide intoxication may appear in tunnels, due to the smoke of the
locomotives using carbon as fuel;
in explosions from the mines, a great volume of carbon monoxide is produced;
in the blood of the big smokers, the CO level may reach 7-8% (the int erior limit of
chronic CO intoxication);
11.2.3.2. Metabolism and mode of action :
carbon monoxide enters in the organism by respiratory way.
it has a great affinity for hemoglobin, bigger than the affinity of the oxygen for
hemoglobin. That is the reason why it can remove the oxygen for hem oglobin. In this
way, hemoglobin becomes incapable to transport the oxygen to tissues. So , the carbon
monoxide intoxication determines a transportation anoxia.
the carbon monoxide elimination takes place by respiratory way, in 12-20 hours. The
elimination occurs faster if oxygen under pressure is administrated.
11.2.3.3. The symptoms in acute carbon monoxide intoxication :
Depends on the carboxi – hemoglobin’s blood level.
The first signs of intoxication appear at 20% carboxi – hemoglobin in the blood
and consist of:
• dizziness;
• headache;
• vomits;
• tiredness;
• visual troubles;
111
• uncoordinated movements, with the impossibility of the victim to goes
out from the room;
• a confusion state, and after it the coma appears;
• The death may appear, by cardiac or respiratory insufficiency . If the
length of the coma is over 5 hours, definitive troubles may appear:
amnesia, confusion state, psychical troubles, paralysis, due to the
cerebral distractions.
• The complications may be precocious, the most frequent being:
pulmonary edema;
bronchopneumonia;
circulatory insufficiency.
At a concentration of 66% carboxi – hemoglobin in the blood, the death occur s
in 5 hours, after a state of coma and convulsions.
At the concentration of 80% carboxi – hemoglobin in the blood, the death is
very fast (flashing); after a few breaths, the convulsions and coma appear.
That flashing death is produced either by the transportation anoxia or the
blockage of the cellular respiratory enzymes.
11.2.3.4. Autopsy appearances :
the skin has a peculiar “cherry-pink” coloration, characteristic for CO intoxication.
This coloration appears only if the saturation of the blood in carboxi – hemoglobin
exceeds about 30%.
the “cherry-pink” coloration is visible also on mucosa, muscles, organs, blood;
congestion and small red spots (small bleedings) are visible under t he mucosa of the
digestive tube, pleura, pericardium, in myocardium, in the white matter of the br ain;
when the surviving period was over 2 days, small necrosis areas appe ar in the brain,
having yellow color and soft consistence. These lesions are present especially in”
globus pallidus”, due to the special irrigation of that part of the bra in and its bigger
necessities of oxygen.
11.2.3.5. The toxicological examination
determines the presence of carbon monoxide in victim’s blood, using a grea t variety of
methods.
carbon monoxide may be determined in a corpse even 1-5 month after the dea th
occurrence.
112
11.2.4. Cyanide Intoxication
hydrocyanic acid is one of the most powerful toxic substance, with a very rapid act ion.
11.2.4.1. Sources of hydrocyanic acid HCN:
it is used like pesticide in agriculture; that is the reason wh y some accidental
intoxications may appear to the person who work in this field, with this kind of
substances;
in pharmaceutical industry- Aqua laurocerasi, containing 1% 0 hydrocyanic acid, is
used for soothing the cough;
in food industry;
in chemical industry, is used for obtaining synthetic fibers;
some derivatives of the hydrocyanic acid was used like fight ga ses during the second
war;
in some countries, it is sometimes used for judicial execution;
a source of intoxication may be the kernels of some fruits, containi ng organic
derivatives of the hydrocyanic acid (for example peaches, plums, che rries, bitter
almonds)
11.2.4.2. By juridical point of view, the death due to cyanide intoxication may be:
Accident:
• to the people who work with this kind of substances.
• an accidental intoxication and even the death may occur to a forensi c
pathologist carrying –out a necropsy of a person who died by cyanide
intoxication, without any protection measures.
Suicide: – to the persons who have access to hydrocyanic acid. Cyani de
intoxication was a suicide method used by the spies during the second war.
Crime: – more rarely hydrocyanic acid was used like an ext ermination method in
the concentration camps, during the second war.
11.2.4.3. Mode of action :
The entrance ways are respiratory or digestive; some derivative s may action on the
cutaneous way also.
The toxicity of the hydrocyanic acid is greater when it enters through respi ratory way.
hydrocyanic acid is a cellular toxic; it determines an using anoxia. It blocks the
respiratory cellular enzymes, especially the cytochrome oxidase.
113
The elimination is made partly by the lungs, and partly it is t ransformed in other
products in the organism.
THE MINIMAL LETHAL DOSE for hydrocyanic acid is 0,05 g when i t enters by
digestive way.
11.2.4.4. The symptoms in acute hydrocyanic acid intoxication :
When the quantity if toxic is massive, the over-acute intoxication occ urs. The death
appears in a few minutes, due to a brutal paralysis of the respira tory centers. The
victim collapses, with convulsions, he loses the conscience and, after s ome
respiratory movements, the death occurs.
In the acute intoxication (the most frequent form):
• firstly, the bitter-acid taste of the hydrocyanic acid is felt;
• large respiratory movements;
• headache;
• sensation of thoracic constriction;
• fear state;
• increased respiratory and cardiac rate;
• at last, apnea occurs, with lack of conscience, convulsions, followed by
respiratory and circulatory paralysis and death. In severe intoxi cation, the
death occurs in 15- 45 minutes. If the intoxication is less severe, the victim
may come to one’s senses in about 1 hour. If the victim survives 1-2 hour s,
the forecast is good.
11.2.4.5. Autopsy appearances :
The external examination:
• the skin has a pink-red color;
• the pupils are dilated;
• the rigidity is powerful and its precociously installed;
• around the mouth and nose of the corpse, a smell of bitter almonds may be
perceived.
The internal examination:
• generalized congestion in the organs;
• mucosal hyperemia
• pulmonary and brain edema;
• red colored blood;
114
• characteristic smell of bitter almonds of the blood and stomach content;
• when the intoxication is due to alkaline cyanide, necrotic lesions of the
internal part of the digestive tube may occur;
• fruit kernels may be found in the stomach if they are involved in the
intoxication.
11.2.5. Corrosive Acids And Alkalis Intoxication
11.2.5.1. Types of actions:
These toxic substances have two kind of action:
Local action – to the contact place, on the skin and mucosa;
General action: – due to the absorption of the toxic;
Local action :
The corrosive acids produce a coagulation necrosis, with the following
characteristics:
• hard;
• dehydration;
• brittle;
• well delimited;
• rough surface;
• The corrosive acids coagulate the proteins, producing necrosis with
different colors, depending on the nature of the acid (for example black-
sulfuric acid; yellow-orange – nitric acid; white-acetic acid; white-gray
– hydrocyanic acid)
Corrosive alkali produce a peculiar form of necrosis, named “meltin g or
softening” necrosis, with the following characteristics:
• thicken aspect;
• soft surface;
• velvet sensation in touching;
• sometimes, pellucid aspect;
• without precise limits;
• around the necrosis area, the tissues have a congestive aspect.
• The corrosive alkali coagulate and dissolve the protein substances. In
time, either acid or alkali produce ulcerations or even perforations, with
115
secondary infections (pleural, peritoneal, mediastinal infections) or the
evolution is towards secondary stenosis.
General actions: t he general actions are due to the intestinal absorption, and are
represented by acidosis or alkalosis with the following consequences:
• respiratory troubles – pulmonary edema;
• circulatory troubles – myocardial paralysis;
• nervous trouble – cerebral edema;
• metabolic troubles.
THE MINIMAL LETHAL DOSE:
• for sulfuric and nitric acids: 10 gr.
• for hydrocyanic acid: 20 gr.
• for the alkaline hydrates: 10-15 gr.
11.2.5.2. The symptoms in corrosive and alkaline intoxications :
after the ingestion of the toxic, powerful pharyngeal and abdominal pains appear. The
ingestion of liquids increases the pain;
difficulty swallowing;
intense thirsty;
vomits with peels of necrotic mucosa, which may have a characteristic smell ;
blood defecation;
bad general state, with: cold perspiration, cyanosis, small pulse, tir edness; the
conscience is preserved.
11.2.5.3. The death is due to:
In the first hours:
• the toxic shock;
• glottis edema;
In the first day:
• the collapse;
After a few days, the death is due to the complications, like:
• bleeding;
• infections;
• perforations;
• nephrosis.
After a few weeks, secondary stenosis may appear, sometimes leading to dea th.
116
11.2.6. Barbiturate Intoxication
The barbiturates are drugs with depressant actions on CNS activity.
They have two main actions:
1. The induction of the sleep
2. Anticonvulsivant action
11.2.6.1. Mode of action :
The barbiturates depress the oxidative metabolism at mitochondrial level.
11.2.6.2. The minimal lethal dose
depends on the type of barbiturate (for example Phenobarbital = 1,8-2 g; cyclobarbital
= 1- 1,5 g).
usually, the minimal lethal dose is 10-15 times bigger than the therapeutic dose.
11.2.6.3. By juridical point of view , the death due to barbiturate intoxication may be:
suicide – frequent, especially in woman, usually in association wit h alcohol
consumption;
accidents – due to confusion, especially in children or overdose in old people;
crime – rarely, because of the big doses which are necessary for death to
occurs;
11.2.6.4. Metabolism of the barbiturates :
The entrance way may be by ingestion or by injection.
The speed of absorption is different, according to:
• the solubility in the organism’s lipids;
• the connection with plasmatic albumins;
• ionization degree.
The degradation takes place mainly in the liver.
The elimination is carried – out by the kidneys.
Due to their metabolism, the toxicity of the barbiturates increa ses in diseases of the
liver and kidneys, and also when the alcohol and barbiturates consumption occurs in
the same time (because both of them are degraded in the liver, at microsomial level).
11.2.6.5. The symptoms in acute barbiturate intoxication :
The symptoms appear shortly after the administration, with digestive and nervous
troubles: dizziness, headache, uncoordinated movements, nausea, and vomits.
After these symptoms, the sleep appears, deeper and deeper, until the profound coma.
117
The coma is calm. With muscular flaccidity, disappearance of th e reflexes, sometimes
the pupils are unequal, cyanosis, dyspneea, congestion of the face, pers piration,
increase body temperature (due to infection or dehydration).Im portant is that all the
troubles due to barbiturate intoxication are reversible, with a proper medical care .
The death may appear and is due to:
• pulmonary edema;
• circulatory collapse;
• pulmonary infections if the victim survives longer.
11.2.6.6. Autopsy appearances :
There are no characteristic autopsy appearances;
The forensic pathologist may see:
• general congestion;
• stasis in the internal organs;
• cerebral edema;
• hemorrhagic areas in the brain;
• inflammatory signs in the stomach’s mucosa;
• sometimes, parts of the ingested pills are found in the stomach;
• in the lungs: stasis, edema, infarction areas, aspects of bronchopneumonia;
• in the cases of prolonged coma, lesions in the liver and in the kidneys may
appear.
11.2.7. Benzodiazepines
Used as anxiolytics, sleep inducing agents, anticonvulsivants, muscle relaxants.
Common brand names: Diazepam, Librium, Oxazepam, Valium, Xanax (stre et names:
Xanax, Tranks, Roofies).
11.2.7.1. Structure: includes a benzene ring fused to a diazepine ring. An aryl ring in the
number five position is required for activity. Chemical substituent’s added to the aryl ring
cause differences in liposolubility, half life and the presence of active metabol ites.
11.2.7.2. Classification:
Short acting – Triazolam – used as a sleep inducing drug.
Medium acting – Lorazepam, Oxazepam – utilized to treat insomnia i n
patients with daytime anxiety.
Long action – Diazepam, Clordiazepoxide
118
11.2.7.3. Absorption : rate of absorption determines the onset of action. The major
determinant of the rate of absorption is lipid solubility. There is considerable range of
lipophilicity (diazepam is the highest).
11.2.7.4. Distribution :
Benzodiazepines are extensively (over 90%) bound to plasma proteins;
Are also highly lipid soluble, and therefore have a large volume of distribution;
Cross the placenta and are secreted into milk;
Drug distribution also determines the duration of action after a single dose.
11.2.7.5. Metabolism:
Benzodiazepines are metabolized by the cytochrome P450 mono-oxigenase system to
active metabolites or inactivated by conjugation with glucuronic acid;
Often benzodiazepines are oxidized to remove an N-alkyl group;
In addition, benzodiazepines can be converted to active metabolites by h ydroxylation
in the 3-position;
Fused ring system also can be metabolized by alpha hydroxylation;
Finally, benzodiazepines are inactivated by glucuronidation.
11.2.7.6. Elimination:
The major determinant of the duration of action of benzodiazepines is the rate of
elimination of the parent molecule and/or active metabolites.
Biologic effects are proportional to the half life of parent compound and active
metabolites. (example: oxazepam – half-life 3-21 hour; diazepam – half-life 20 – 100
hour)
11.2.7.7. Potential medical problems with benzodiazepines:
Toxicity of benzodiazepine is low.
They act synergistically with other CNS depressants (ex. Alcohol, other depr essant)
Diazepam toxic level > 5 ug/ml
Toxicity is characterized by lethargy, coma, confusion and respir atory depression that
is the most important effect.
11.2.7.8. Dependence and withdrawal:
Benzodiazepines have a significant potential for abuse and can cause p hysical and
psychological dependence.
Abrupt cessation after prolonged use causes a withdrawal syndrome.
119
Withdrawal symptoms include anxiety, insomnia, headache, dizziness, vomit ing,
weakness, irritability, hypersensitivity to visual and auditory stimuli, palpitation,
tachycardia and postural hypotension.
In severe and rare cases of withdrawal from high doses, patient m ay develop affective
disorders or motor dysfunction: seizures, psychosis, agitation, confusi on and
hallucinations.
11.2.7.9. Treatment of overdose:
Vomiting should be induced
Activated charcoal should be given to reduce absorption.
Flumazenil may be useful as an antidote.
11.2.8. Pesticides Intoxications
The main danger from agricultural chemicals lies in the pesticides.
Pesticides are a general name, including a great number of subst ances used for the
protection of the cultures against the deleterious organisms.
By juridical point of view , the death due to the pesticides may be:
Accident – is the most frequent, especially in domestic medium, in persons who
manipulate these substances or by consuming the products treated rece ntly with
pesticides;
Suicide – is frequent, especially in rural medium, due to the easy a vailability of
these substances;
Crimes – especially with parathion and stricnine.
The symptoms in acute pesticides intoxication , the common symptoms, for all the
pesticides are:
• digestive troubles –the common entrance way for the pesticide is the digestive
one;
• nervous troubles;
• cardiac and circulatory troubles;
• respiratory troubles;
• lesions of the liver, kidneys, skin;
• blood changes;
• enzymatic, metabolic and biochemical troubles;
One of the most common pesticides, involved frequently in acute intoxica tions are the
organo-phosphorus compound and, from these the parathion.
120
11.2.9. Parathion Intoxication
11.2.9.1. Metabolism :
Entrance ways:
• cutaneous;
• digestive;
• respiratory;
The degradation of the parathion takes place in the liver, by its t ransformation in
paraoxone, a more toxic agent.
The elimination is by the urine, where we may find only a product of degradation:
paranitrophenole.
The minimal lethal dose is of 0,20 – 0,50 pure parathion .
11.2.9.2. The mode of action and symptoms :
The parathion inhibits the cholinesterase of the organism, producing the a cetylcholine
accumulation.
The result is the apparition of three groups of symptoms:
Muscarinic effects:
• abdominal pains;
• vomits;
• perspiration;
• increased salivary and bronchial secretion;
• urinary incontinence;
• dilatation of the pupils.
Nicotinic effects:
• muscular fibrillation at the muscles of face, tongue, neck;
• muscular contractions, with sensation of thoracic constriction;
• after a period of time, the muscular flaccidity appears and the pa ralysis
occurs;
CNS effects:
• restless;
• fear;
• headache;
• dizziness;
• mental confusion;
121
• slumber;
• ataxia;
• convulsions, coma.
The death is due to respiratory troubles, by:
• bronchial constriction;
• blockage of the respiratory muscles;
• bronchial hyper secretion;
• inhibition of the respiratory center.
11.2.9.3. Autopsy appearances:
The external examination:
• a characteristic sign is myosis, which may disappear during the agonia;
• cyanosis;
• precocious rigidity;
The internal examination:
• pulmonary edema;
• generalized stasis;
• the characteristic content of the stomach: green color if the product was
previously colored and also a characteristic smell of garlic.
11.2.10. Narcotics/Opioids
In the legal classification the term narcotic includes drug wi th morphine-like
activity as well as marijuana. In medicine/toxicology the te rm opiates is used to designate
the morphine-like drugs.
The classification of opioids on the basis of their source:
Natural opioids: morphine and codeine;
Semisynthetic opiods: heroin, hydromorphone (Dilaudid), oxicodone (Percodan),
dextromethorphan.
Synthetic opioids: meperidine (Demerol), diphenoxylate (Lomotil), met hadone
(Dolophine), pentazocine (Talwin).
11.2.10.1. Morphine
A potent narcotic analgesic and its primary clinical use is in the management of
moderately severe and severe pain.
Trade names: Roxinal, Duramorph, Morphine Sulfate;
Street names: Miss Emma;
122
Physical appearance :
Legally available only in the form of its water – soluble salts: most common are
morphine sulphate and morphine hydrochloride.
Both are fine white crystalline powders, bitter to the taste, sol uble in water and slightly
soluble in alcohol.
Routes of administration and absorption :
May be taken orally in tablet form (it is an impractical route for abuses because it costs
too much, resultant peak blood levels are only one tenth as high as givi ng the same
amount parenterally)
Injected subcutaneously, intramuscularly or intravenously (the route pre ferred by
abusers)
After absorption morphine is rapidly distributed throughout the tissues wi th the highest
blood flow (lung, kidney, liver, spleen, muscle)
Dosage:
For moderate to severe pain the optimal intramuscular dosage is cons idered to be 10
mg per 70 kg body;
Intermittent users may use doses within the therapeutic range
Regular users frequently increase the dose as tolerance devel ops. To take several
hundred milligrams per day is common.
Metabolism:
The principal site of metabolism is the liver:
Most morphine (half-life 2 hours) is metabolized by glucuronidation, bei ng converted
to its principal metabolite morphine-3-glucuronide 50-60% (half-life 4 hours) and
smaller amounts of morphine-6-glucuronide 15% (half-life 3 hours)
Normorphine is another metabolite. Large amounts are produced after ora l
administration. This compound is both psychoactive and neurotoxic.
Once morphine has been converted to the glucuronide, excretion is through urine
Less than 10% of a given dose is excreted unchanged in the urine.
Detection:
Given current levels of sensitivity, morphine and its metabolites should be detected for
at least 48 hours after administration
Can be detected in urine.
11.2.10.2. Heroine (diacetylmorphine)
Has no legitimate medical uses and is only available illegally.
123
Street names: Horse, Smack.
It is produced by the acetylation of morphine’s two hydroxyl groups.
Route of administration:
Heroin is usually injected, but may be smoked or snorted. Heroin can be heated on
piece of folded tinfoil and the fumes inhaled.
Insufflated doses of heroin are 5 – 20 mg of pure heroin and intravenous dose s are 5 –
10 mg.
As usage increases, however, the doses get much higher (2 grams per day).
Metabolism and elimination :
Heroin is rapidly deacetylated to 6-acetylmorphine or 6-monoacetylm orphine, and
therefore heroin itself is rarely ever detected in the urine.
6-AM is rapidly deacetylated to morphine. Heroin has an analgesic ef fect attributed to
6-AM and morphine.
Elimination is mostly in urine: 1,3% 6-AM, 4% morphine, 38% morphine conjugate ,
0,1% heroin. Detection of 6-AM in the unique identifier of heroin usage.
Mechanism of death: respiratory depression, pulmonary edema.
11.2.10.3. Marijuana
Cannabis is a leafy plant which grows wild in many of the tropic and tempe rate areas
of the world. It is cultivated both indoors and out for the production of it s flowering
tops.
The most commonly used form of cannabis are the leaves and flowering tops. It also
comes in a more concentrated resinous form called hashish, and as a sticky bla ck liquid
called hash oil.
The term ‘hemp” is generally used to describe low-the varieties of cannabis which are
grown for industrial uses.
Delta 9 tetrahydrocannabinol, the most psychoactive chemical in the cannabis plant, is
found in the plant’s resin. The resin is most concentrated in the flowers.
Street names: Blunt, grass, Herb, Pot, Smoke, Weed.
Medical use:
Marijuana’s healing nature for AIDS and cancer is a res ult of its ability to increase the
appetite as well as relieving nausea allowing the patient to regain weig ht.
Reduces ocular pressure in glaucoma.
Routes of administration:
Marijuana is usually smoked;
124
A single intake of smoke from a pipe, water pipe, or joint is generally called a hi t;
The strength of cannabis varies greatly from one variety to anothe r. Generally 3,5 g of
mid-quality bud could get around 20 – 30 people reasonably high;
Marijuana sometimes is eaten;
Peak levels within 15 min of smoking 50-70ng/ml
5-10 ng/ml induce no effect to impaired function;
Absorption and distribution:
Transpulmonary absorption rapidly gets psychoactive drugs to brain;
The drug is slowly absorbed from the gastro-intestinal tract;
THC leaves the bloodstream and is distributed into different parts of the body where it
is metabolized, excreted and stored.
Metabolism and elimination:
THC is metabolized in the liver – half-life 30 hours;
However, the liver is not able to metabolized the THC very quickly, the unmetabolized
THC binds to the fat cells in the body. Between periods of active m arijuana use, the
fat-bound THC is slowly released back into the blood.
Principal metabolite is hydroxyl product at C11;
Metabolites transformed by alcohol dehydrogenase to carboxyl der ivative that is
excreted in urine;
50% of doses is excreted following oral dose in 3 days;
Repeated use of marijuana results in induction of metabolizing enzymes.
Mechanism of toxicity:
There is a cannabinoid receptor in the brain;
The brain has its own compound –anadamide- which binds with cannabinoid receptors;
Another compound called 2-AG also activates the THC receptor in the brain;
The hippocampus of the brain has a very high concentration of cannabinoid r eceptors.
It is critical to the formation of new memories, not surprisingly , the inhibition of
memory formation is the most well-establised negative effect on mental function of
marijuana.
Symptoms:
The effects of smoked cannabis peak after about 20 minutes and last for 1-2 hours,
when eaten, the effects will peak more slowly and primary effec ts may last for 3-4
hours.
125
The effects of smoking cannabis are usually lighter than those of many other
recreational psychoactive substances. People are generally capable of carrying out
normal actions and activities while high.
Relaxation, stress reduction creative, philosophical or deep thinking, ide as flow more
easily. Pleasant body feel. Increase in body/mind connection pain relief.
Nausea coughing, asthma, upper respiratory problems difficulty wit h short term
memory during effects and during periods of frequent use racing he art, agitation,
tenseness mild to severe anxiety panic attacks at very high dos es or in sensitive users
headaches dizziness, confusion paranoid and anxious thoughts more frequent; pos sible
psychological dependence on cannabis.
“a motivational syndrome” from chronic marijuana use marked by apa thy, dullness,
diminished goal-directed activities, impaired concentration and deteri oration in
personal appearance.
Increase pulse rate, photophobia, reddened conjunctiva, decreases intraocul ar pressure.
Alteration of mood, sensory perception, lethargy, increased appetite.
Toxicity:
Serious symptoms primarily occur in children: stupor, tremor, low blo od pressure,
tachycardia.
There are no confirmed, published deaths from cannabis-only poisoning.
There are a small number of people who report serious cannabis all ergies which cause
unexpectedly intense reaction, throat and lung irritation, etc.
Tolerance and withdrawal:
In addition to tolerance a mild abstinence syndrome may follow abrupt termination of
very high dose, chronic marijuana use.
Symptoms include : irritability, sleep disturbance, diminished appetite, gastro-
intestinal distress, sweating, and tremors.
Mild withdrawal syndrome occurs after cessation of high-dose, c hronic THC use. It is
characterized by 4 to 5 days of irritability, restlessness, ner vousness, decreased
appetite, weight loss and insomnia.
11.2.11. Stimulants
Agents that can stimulate the CNS from mild hyper excitability to severe convulsions
126
11.2.11.1. Cocaine
An alkaloid extracted from the coca plant, erythroxylon coca, a shrub native to eastern
side of Andes. Is abused for it stimulant properties. Medical use: topical application as
a local anesthetic in ear, nose and throat surgery and in ophthalmological procedures.
Street names: Coke, snow, rock, crack.
Physical and chemical properties:
It is usually obtained as cocaine hydrochloride.
Those who smoke the drug prepare the free base or crack form, chemi cally removing
the hydrochloride.
Crack cocaine is processed with ammonia or sodium bicarbonate and wate r and heated
to remove the hydrochloride, thus producing a form of cocaine that can be smoked.
The term “crack” refers to the crackling sound heard when the mixture is smoked.
Routes of administration:
Snorted intranasally 2 – 3 lines of cocaine (approximately 100 mg) g ive blood levels of
0,5 – 0,10 ug/ml, onset of action is 30 seconds – 2 minute.
Intravenous injection of this same amount results in peak levels of 0,70 – 1 ug/ml,
onset of action 15 seconds or less, peaks in 3 – 5 minutes and lasts 15 – 20 minutes.
Cocaine injection may be mixed with heroin to make “speedballs”
Smoking 50 mg of crack (16 – 32 mg of cocaine) gives levels of 0,25 – 0,35 ug/ ml,
onset of action is 10 seconds or less, peaks in 3 – 5 minutes and lasts about 15 minutes.
Metabolism:
Cocaine is rapidly cleared from the blood stream.
Half-life – 40 minutes.
Benzoylecgonine (BEG) and ecgonine methyl ester (EME) are c ocaine’s principal
metabolites.
Both hepatic esterases and plasma colinsterases convert cocaine to EME.
Benzoylecogonine forms spontaneously.
The half-life of both metabolites are much longer than the half-lif e of the parent
compound.
Cocaethylene – is produced only in the presence of ethanol. Is synt hesized in the liver.
It crosses the blood brain blood barrier easily and binds to the dopamine receptor with
the same affinity as cocaine. Is more lethal than cocaine.
127
Mechanism of toxicity:
Inhibition of the dopamine reuptake transporter in the nucleus acumens in br ain
accounts for intense euphoria and reinforcing property of cocaine.
Cocaine, particularly crack, is the most addictive of all mood-alte ring substances due
to rapid onset of intense euphoria, short half-life (40 to 60 minutes) and intense
dysphoria and craving following the high.
Cocaine intoxication:
Increased temperature, dilated pupils, vasoconstriction, hypertensi on, mental alertness,
increased energy, decreased appetite, increased heart rate.
Cocaine induces mental confusion or hallucinations, overdoses cause seizur es,
respiratory depression, cardiac arrhythmias, myocardial infarction and dea th.
Mood disturbances, lethargy, exhaustion, impaired judgment, changes in sociabilit y.
Respiratory depression at toxic levels.
Vasoconstriction and decreased force of heart contraction, increased heart rat e.
High body temperature.
There is for the most part no lethal level of cocaine. Some individua ls die at levels that
are recreational for other individuals.
The mechanism of death is a fatal cardiac arrhythmia, acute myocardia l infarction.
Cocaine withdrawal:
Dysphoric mood (an unpleasant mood including anger, irritability, sadness, a nxiety,
fear, restlessness), fatigue, vivid and unpleasant dreams, insomnia, ps ychomotor
retardation.
Treatment:
Remove the oral cocaine by emesis or charcoal lavage.
Supportive care for respiration and circulation.
Return the body temperature to normal to reduce incidence of convulsions.
11.2.12. Hallucinogenes
The term designates a drug that acts on the CNS to produce a sta te of perception of
objects with no reality or of sensation with no external cause.
11.2.12.1. LSD – Lysergic Acid Diethylamine
A semi-synthetic compound derived from the fungus ergot, which grows on rye. The
most potent hallucinogen.
Street names: acid, cid L, blotter, LAD, trips.
128
Physical properties:
LSD is initially produced in crystalline form.
The pure crystal can be crushed to powder and mixed with binding agent s to produce
tablets known as “microdots” or thin squares of gelatin called “window panes”; more
commonly it is dissolved, diluted, and applied to paper or other materials.
Routes of administration and absorption:
It is usually ingested in the form of impregnated paper or sugar c ubes, capsules and
tablets.
The standard street dose is 100 – 300 ug.
Intravenous use is rare.
The physical effects of LSD are seen within 20 minutes; psychoa ctive effects occur
within 2 to 4 hours.
Absorption is rapid and almost complete.
Is rapidly absorbed from the gastrointestinal tract, and quickly dist ributed to all body
tissues including the brain.
Metabolism and elimination:
Metabolism is primarily via hydroxylation and conjugation in the live r, with
conjugates excreted in feces.
Has a half-life of 2,5 hours.
Mechanism of toxicity:
Acts as serotonin agonist.
There are two major groups of serotonin receptors (serotonin 1 and serotonin 2).
LSD acts on both types of receptors – it blocks one while stimulating the other.
The stimulated serotonin 2 receptor is important for hallucinogenic activity.
Most of these receptors are in the cerebral cortex.
Symptoms:
LSD usage results in perceptual and psychic symptoms.
LSD causes dramatic changes in perception, thought and mood.
There may be vivid pseudo-hallucinations that users are aware are not real.
There is distortion of time, distance and gravity.
LSD users may experience synaesthesia – this is the perceptua l impression that they
are hearing colors or seeing sounds.
There is a diminished control over thought processes resulting in rec ent or long-
forgotten memories resurfacing.
129
There are feelings of mystical, religious or cosmic enlightenment.
Acute adverse effects: pupil dilation, difficulty focusing, increa sed salivation, slight
increase in body temperature and in heart rate anxiety, tension, increased perspiration,
nausea, dizziness, confusion, paranoia, fear, and panic, unwanted and overwhelmi ng
feelings, flashbacks.
LSD flashbacks (post-hallucinogen perceptual disorder) a recurrenc e of the drug-
induced state, may be pleasurable or distressing. Flashbacks are usually br ief; they may
be precipitated by stress, fatigue and certain drugs such as marijuana.
Chronic adverse effects include a prolonged psychotic state resembli ng schizophrenia
or mania, depression, chronic anxiety and chronic personality changes.
Tolerance and withdrawal:
There is no known pharmacologically lethal dose of LSD.
Tolerance to LSD’s psychoactive effects builds rapidly so that a dose taken three or
four days running will, by the fourth day, produce no trip. Abstaining for s everal days
will allow the sensitivity to return.
LSD is quite unlikely to lead to addiction in most people. There is no ph ysical
addiction or withdrawal after heavy use, although people can and to become mentally
habituated to LSD as with any substance.
11.3. Investigation Of Drug Abuse Death
11.3.1. Scene:
The dead person’s clothes should be examined and described for drugs in t he pockets
or hidden in seams, belt, shoes, money purse, eye-glasses case, jew elry, etc. The body
should be examined for caches of drugs that may be in body orifices, taped to the body
between buttocks, toes, under the breasts or attached to a string ti ed around a tooth and
then swallowed. Rarely, the needle, syringe and tourniquet may be found i n place on
the body. The tourniquet may contain concealed drug. Sometimes, the clot hing and the
body may be tampered.
Photographs of the scene and surrounding objects should be taken. Psychedeli c posters
may suggest drug abuse. The surroundings should be searched and any dr ugs found
preserved. A needle and syringe, a cooker, and a source of heat are usually present.
The contents of the cooker should be sent for analysis. Tubes of plastic glue or plastic
bags indicate death due to a volatile, such as glue or solvent. Aerosol cans and ball oons
indicate “huffing” death.
130
11.3.2. Apparatus and Preparation of Drugs for Injection:
Illicit narcotics are purchased “on the street” as packets o f powder, tablets or capsules
containing the alkaloid (usually four to eight percent), which has been di luted (cut) by
quinine, mannitol, lactose, etc.
The powder is placed with water in a small receptacle, e.g. bott le cap or spoon
(cooker), which is heated until the powder dissolved. The solution is then dr awn into a
standard or improvised syringe, usually through a bit of cotton to filter out insoluble
particles. Belts or elastic bands are used as tourniquets.
11.3.3. Autopsy:
11.3.3.1. External:
There is often wasting and signs of self-neglect. The body ma y be extensively tattooed
and hide scars. Stains may be found on the tips of fingers, indicati ng the possible type
of pill or capsule handled. Linear needle track scars, often pigme nted are usually found
overlying fibrosed veins of the antecubital fossae, forearms, and dors a of the hands in
“main-liners”. Sometimes, needle tracks are found on scalp, neck, subli ngual areas,
shoulder, inguinal region, penis, vagina, popliteal area, ankle and foot. Punc tuate areas
of black discoloration (soot tattooing) are caused by deposition of ca rbonaceous
materials along the track of the needle. Such tattooing is cal led “turkey skin”, as it
resembles the plucked bird. Customary target areas for subcutaneous or intramuscular
injection are the upper arms and thighs. Recent injection sites ma y show zones of
inflammation surrounding or adjacent to a needle puncture site. The i nflammatory foci
may resolve leaving no trace, or may form abscesses or ulceration.
Chronic edema of the hands, secondary to occlusive thrombophlebitis in the forearms,
is seen occasionally in long term addicts. A single fresh needl e puncture shows a tiny
crusted focus, but may be difficult to identify, but incision through the skin may show
a perivenous hemorrhagic track. The subcutaneous heroin users show a hi gher
incidence of abscess. Healing by fibrosis may produce hyperpigmente d macules or
retracted, circumscribed scars which resemble those from sm allpox vaccinations.
Additional damage to the skin and subcutaneous tissues results from atte mpts by the
addict to obliterate the track by overlaying it with a cigaret te burn or abrading with
pumice stone, sandpaper or using escharotics chemicals. The regional lymph nodes
may be enlarged.
131
Habitual inhalation of cocaine or heroin (snorting or sniffing) cause p erforation of the
nasal septum varying in size from a pinhead to several centimet ers. They may be
round, oval or irregular. Froth may be seen at the mouth and nose.
11.3.3.2. Internal:
Gastrointestinal tract may contain pills or capsules.
Microscopic examination of section of stomach polarized light someti mes shows
particles of optically active filter material (example: s tarch, talc, cellulose) adherent to
the gastric mucosa in victims of fatal drug ingestion.
Needle scars show perivenous fibrosis in the intravenous addict and a cute or chronic
abscesses, or diffuse subcutaneous scarring in the skin popper.
Microscopic examination often shows foreign material in the scar tissues, example –
fragments of cloth, cotton, talc or unidentifiable matter with surroundi ng foreign body
giant cell reactions. Repeated injections can give rise to a chr onic myopathy which is
in part due to chronic infection, but is exacerbated by an autoimmune r esponse to
damaged muscle. Histologically, affected areas show fiber nec rosis, replacement
fibrosis and infiltration by polymorphs and lymphocytes which extends f ar beyond to
area of the injection. To examine the veins, make a single longitudina l incision of the
flexor surface of each arm from mid-biceps to distal forearm . The incised margins are
reflected widely to expose subcutaneous tissues and veins. To reduce a rtefactual
hemorrhage, this should be done after thoracic viscera have been rem oved. There may
be phlebitis, phlebosclerosis, thrombosis, and recent and resolving perivenous
hemorrhage. The vein and surrounding tissue should be preserved for chemical
analysis.
The most common internal pathologic changes from parenteral drug abuse consist of
hepatic lymphadenopathy, and hepatic portal triads. Enlarged lymph node s at the porta
hepatis, adjacent to the common bile duct and at the pylorus of the st omach usually
measure three to four cm. Microscopically, such lymph nodes show non-speci fic
hyperplasia. Dense lymphocytic infiltrates involve all of the port al triads, with or
without parenchymal pathologic stigmas of viral hepatitis.
Typical visceral anatomic findings include the non-specific pulmonary triad of edema,
bronchopneumonia, and aspiration of gastric contents. Froth is present in t he upper
respiratory tract, which comes out from the nose and mouth. In mainline rs, the crystals
lodge in pulmonary capillaries, and produce a foreign body granulomatous reaction.
Such granulomas erode the walls of capillaries and unite, forming la rger granulomas.
132
In extreme cases, the lungs have a multinodular, gritty texture, and microscopic
examination under polarized light shows large quantities of talc, st arch or cellulose in
these lesions. Pulmonary hypertension with right ventricular cardiac hypertrophy
occurs due to extensive microcrystalline pulmonary emboli. Most heroin addicts have a
few optically active crystals in their pulmonary capillaries. Pleurae may show petechial
hemorrhages. The lungs are usually congested and oedematous. Liver may be slightly
enlarged or shows evidence of cirrhosis. The heart may show valvula r diseases.
Pericardial, pleural and peritoneal effusions may be fund. The bra in may show oedema
and focal areas of necrosis involving the globus pallidus and hippocampus due to
hypoxia. Hyperplastic changes in the reticuloenondothelial system are common.
Splenomegaly and portal lymph nodes hyperplasia are common. The most cons tant
finding in both spleen and portal lymph nodes is the presence of large germinal cente rs,
but the morphological features are not specific. Birefringent m aterial is present in
spleen more often than in portal lymph nodes. Lysozyme containing cells are found in
the spleen indicating bacterial contamination. The presence of signif icantly more IgM
and IgC containing cells in spleen and portal lymph nodes indicates a cute, subacute
and chronic antigen stimulation.
11.3.4. Complications of Drug Misuse:
Drugs of abuse may be taken by injection (intravenous, subcutaneous or rarely
intramuscular) by sniffing into the nostrils, through rectum or v agina, by inhalation,
smoking or orally.
These different routes may produce different physical lesions.
Self-neglect, malnutrition, dental decay.
Complications of injections:
• The veins in the arms, hands, legs and sometimes abdomen, groin or
neck are damaged. Over-use of the same veins produces thrombosis and
phlebitis, especially if the substance is irritative or unsteril e and
pulmonary embolism. The veins become dark in color, may be hand and
cord-like due to thrombosis and fibrosis, and may ulcerate. When
healed, there may be white or silvery linear scars in the axis of the limb.
• Fragments may be injected which lead to microemboli in the lungs and
liver, where they form granulomas or abscesses.
• Intra-arterial injection may cause vascular damage and gangrene.
133
• Infection: cellulitis and abscess formation at the injection si t, and
depressed areas of fat atrophy may be present.
• Fat necrosis and chronic myositis may be seen. Septicaemia a nd
subacute bacterial endocarditis may occur.
• Inhalation may precipitate asthma or bronchitis, pneumothorax,
pneumomediastinum, and vomiting.
• Shared syringes and needles can transmit hepatitis B and C, HIV,
syphilis and malaria.
Acute and chronic liver disease.
Kidney problems and amyloidosis.
Psychiatric complications.
Tuberculosis and pneumonia due to reduced resistance and poor nutrition.
They are more commonly involved in various accidents due to impairment of
alertness and behavior.
The need to obtain money may lead to squalor, theft and prostitution.
Personal violence and murder is more common.
Acute myopathy, meningitis, brain and pulmonary abscesses, various
neurological abnormalities, acute muscle necrosis with myoglobinuria and rena l
failure are rare complications.
Death can occur due to overdose or from contaminants.
11.3.5. Over dosage and hypersensitivity:
Death can occur rapidly, especially with i.v. use of heroin. Due to hypersensitivity,
sometimes a first time user may die rapidly and the needle and syringe may be found in
the vein.
Death appears to be due to acute left ventricular failure and gross pulmonary edema.
Froth may be seen exuding from the mouth and nose.
134
CHAPTER 12: FORENSIC PSYCHIATRY
12.1. General aspects: mental illness
Psychiatry deals with the study diagnosis and treatment of ment al illness. Forensic
psychiatry deals which application of psychiatry in the administra tion of justice. Insanity
or unsoundness of mind can be defined as a disease of the mind or the per sonality, in
which there is derangement of the mental or emotional processes. T he intelligence is
weakened or perverted, but the insane person may not show physical wea kness. The law
has not defined insanity. The term is used for those persons who are una ble to adopt
themselves to the ordinary social requirements, due to mental disea se. The law is most
frequently concerned with “mental impairment” and not “mental illne ss”. Different kinds
and degrees of mental impairment are required for different legal issues. The following are
some of the important terms in connection with insanity.
An abnormal mental state may be due to a functional psychotic, to s ubstance misuse,
to an abnormal metabolic state, such as hypoglycemia, or due to les s common problems,
such learning disability, and organic brain disease or head injury. In abnormal menta l state,
the effects of stress anxiety fear or anger may coexist w ith intoxication (hallucinogenics
and stimulants) of some kind and the behavior, demeanor and appearance shoul d be
observed.
12.2. Medico-legal psychiatric examination
Is carried out in several situations:
a. For the adult defendant:
– When he has an abnormal behavior during the juridical investigation;
– If the defendant, before the delict, a disease or a trauma which c an produce
psychiatric disorders (for example – a cranio-cerebral trauma);
– When the murder is done without any obvious reason or with extremely cruelty.
b. For the under-aged persons involved in a delict.
c. For suspending the execution of the punishment, when the mental disorder c annot
be treated in the penitentiary hospital.
d. For raising the security measures proposed by a former examination.
e. For cancelling the marriage if the wife or the husband has a mental disease .
135
f. For establishing the validity of an act (for example testament).
g. For estimating the psychiatrical invalidity or infirmity.
h. For establishing the capacity of a person to have a driving license.
i. For establishing the possibility of a person to have a certain job.
j. For establishing the psychical sex and for changing the civilia n sex to a
transsexual.
k. For entrusting the under-aged children to education.
The purpose of the psychiatrically medico-legal examination is to establish the
judgment of the person
The judgment is the capacity of a person to realize his action s and also to realize the
consequences of them (juridical definition)
The judgment is the capacity of a person o distinguish between permitted and non-
permitted, right and wrong, fair and unfair, and so on (the medico-legal definiti on)
The judgment is a medico-legal term; the juridical equivalent i s the responsibility
(“the responsibility is the face to the world of the judgment”)
There are 3 types of judgment:
1. Present – the defendant has penal responsibility.
2. Diminished – the defendant has diminished penal responsibility.
3. Absent – the defendant has no penal responsibility.
From the ancient times, example in the Roman Penal Code, the person with a mental
disorder is not penal responsible, depending on the degree of the mental disorder.
12.3. Types of abnormal mental condition
The spectrum of behavior in the “normal” population is so wide that a definition of
what is abnormal is hard to express, especially as it varies g reatly with ethnic, social,
religious, national and geographic influences.
Probably, abnormal behavior or “disorders of the mind” can best be assume d when it
becomes unacceptable to the rest of the community.
Mental abnormal may be:
• Congenital – mental defect, impairment, handicap or under normality.
• Acquired – mental disease or illness.
These categories are not sharply divided or it is probable that som e mental disease,
such as schizophrenia, have a congenital origin, even if the manifestations are dela yed.
136
12.3.1. Mental under normality
Provides a wide range of severity depending on I.Q.
There are three degrees of mental under normality:
a. I.Q. under 70 – the easy form – with mental age about 10 years. In these mental
defectiveness, not amounting to imbecility exists from birth or an early age and
they require care, supervision and control for their protection.
b. I.Q. under 50 – mental age about 5 – 7 years – called also the imbecili ty. These
persons are incapable of managing themselves or their affairs. An imbecile is
incapable of being taught.
c. I.Q. under 40 – the severe form, with mental age about 3 – 5 years – cal led the
idiot. The idiot is characterized of incomplete maturation of attent ion, perception,
cognition and social adaptability due to arrested mental development . It results
from environmental, genetic, endocrinal (thyroid deficiency) meta bolic
(galactosemia, porphyria, neurolipidoses, hepatolenticular degeneration) infective
(congenital syphilis, toxoplasmosis, meningitis, encephalitis) and birth trau ma.
Medico-legal aspects o mental subnormality:
• The person with mental subnormality is mostly involved in thefts an d sexual
offences, frequently leaded by a person with a normal I.Q because the persons with
mental subnormality are very influenced.
• The judgment is present or diminished in the mental subnormality of first degree,
in the second degree is diminished or absent (depending on the situa tion in which
he commited the felony) and in the third degree is absent.
12.3.2. The psychopathic personality
It is difficult to be categorized into congenital or acquired. In man y ways, it is not a
mental defect alt all, but one extreme of the spectrum of variation in individual pers onality,
in the individual retaining a childlike selfishness. They have no a bnormality of thought,
mood or intelligence (usually I.Q is normal), but their unacceptable b ehaviors marks them
out as “psychopaths”.
Psychopath or sociopath is a person who is neither insane nor mentall y defective, but
fails to confirm to normal standards of behavior. Psychopaths have abnorm al personality,
persistently behave in an antisocial or disruptive manner, and are una ble to appreciate the
137
moral implications of their actions. It is not a ground for an insani ty defense, but may
provide a plea of diminished responsibility. In this there is a fai lure of maturation of the
personality, the individual retaining a child-like selfishness.
The psychopathic personality is characterized by:
• Lack of emotional responses.
• An unswerving desire for the gratification of their desires.
• Complete lack of conscience.
That is why, frustration of any whim is not tolerated and is foll owed by aggression,
completely devoid of any regret or remorse. Their defect appears to be morta l.
Immediate violence, including murder, may arise from as, challenge to their eg oism.
They are dangerous people, because their intellect is almost norm al, thus they can plan
and implement their anti-social acts, often criminal activities in a perfe ctly efficient way.
The judgment is present in the majority of cases, but there are situation with
diminished judgment depending on the circumstances of the delict (the rol e of the victim
must be estimated).
12.3.3. Mental illness
Acquired or appearing after childhood, comprise several major groups:
12.3.3.1. Organic psychoses
Mental illnesses which arise from some structural brain dama ge are called organic
psychoses. The organic psychoses are characterized by liability of mood, failure of
memory, deterioration of intellect, irritability, irrational ange r, confusion, loss of social
inhibitions, which may lead such persons into unacceptable behavior and eve n sudden
violence.
12.3.3.1.1. Pre-senile Dementia :
Dementia is a condition in which there is degeneration of mental f aculties after they
have been fully developed. The effect on the brain is widespread with l oss of intellect
and memory, together with disturbance of emotion and of behavior. Including:
Alzheimer’s disease; Pick’s disease; Creutzfeldt-Jacob disease Hunti ngton’s chorea.
12.3.3.1.2. Senile Dementia:
It is caused due to arteriosclerosis and old age. It usually sta rts after 65 years. A feeling
of loneliness, of being unwanted, loss of prestige and death of a close relative cause the
onset of the disease. The patient is confused, judgment and memory is i mpaired.
138
Delusions, hallucinations and emotional outbursts are common. The medico-leg al
problem may be represented by the difficulties over the dispositi on of property
(testamentary capacity). These person have the judgment present, diminishe d or absent,
depending on the stage of pathological process which lead to the mental disorder.
12.3.3.1.3. Cerebral Tumors:
Mental symptoms may occurs at any stage of growth of cerebr al tumors involving
prefrontal, frontal, temporal an parietal lobes.
12.3.3.1.4. Cerebral Trauma:
It causes concussion and post-traumatic automatism. The late effe cts are: intellectual
impairment, emotional changes and epilepsy. Cerebral trauma can prec ipitate any type
of mental illness.
12.3.3.1.5. Drug-induced Psychosis :
Dependence on barbiturates, amphetamines, cannabis, heroin, cocaine leads to
psychosis. Cocaine, LSD, amphetamines and mescaline can produce clinic al symptoms
similar to schizophrenia.
12.3.3.1.6. Toxic Psychosis :
Heavy metals, such as arsenic and mercury any produce mental degeneration.
12.3.3.1.7. Alcoholism :
• Alcoholic Blackouts : These are episodes of amnesia of several hours for
events which have occurred during a drinking session. Grossly abnormal
behavior or criminal acts may be committed during these episodes.
• Delirium Tremens : Is usually occurs in a chronic drunkard: one to two
days after sudden withdrawal of alcohol; due to heavy drinking; injuries ,
infection and shock act as precipitating agents. This is the commonest type
of psychosis in the chronic alcoholic. The patient becomes sleepless,
restless and irritable and then develops disorders of perception and coa rse
muscular tremors of face, tongue and hands. Disorientation and
hallucinations of sight and hearing are common. He may be incited t o
commit suicide, homicide or violent assault. Symptoms usually last f or
three to seven days. Such persons are not criminally responsible.
• Alcoholic Hallucinosis : The patient suffers from illusions and
hallucinations which can lead to eccentric behavior.
139
• Korsakov’s Psychosis : It is characterized by loss of memory for recent
events both retrograde and anterograde. Affected individuals remain
responsive and alert despite the severe memory and learning impai rment.
The physical component of this syndrome consists of ophthalmoplegia,
ataxia and peripheral neuritis and is known as Wernicke’s encephalopathy.
• Delusions of Jealousy : Chronic alcoholics often become suspicious and
paranoid especially when they are drunk. They develop delusions of
infidelity and jealousy which may lead to violence and murder.
12.3.3.1.8. General Paralysis of the Insane :
This is a chronic progressive condition leading to paralysis a nd dementia. It is usually
associated with meningovascular syphilis and tabes dorsalis. There i s a chronic
psycho-organic syndrome characterized by temperamental and per sonality changes the
memory is impaired and thought retarded.
12.3.3.1.9. Epileptic Psychosis :
Short transitory fits of uncontrollable mania occur. There is ge neral impairment of the
mental faculties with loss of memory ad self-control. Auditory a nd visual
hallucinations are followed by delusions of persecution. Moral sensibil ity is lost and
sometimes they are dangerous to themselves and to others. These may be progressive
dementia.
• Pre-epileptic Insanity : Instead of epileptic aura, the patient may
occasionally develop violent fits of mania or extreme depression of mind.
Hallucinations and delusions are common during this stage, and such
persons may commit assault or other criminal acts.
• Post-epileptic Insanity : The stupor following epileptic fit is replaced by
automatic acts, of which the patient has no recollection. The patient is
confused and terrified by visual and auditory hallucinations and delusions
of persecution, and may commit crimes like thefts, conflagration, sex ual
assaults and murders. These crimes are involuntary, automatic and
unpremeditated. The patient never attempts to conceal them on regaining
consciousness. Automatic action tends to be of the same type in each
attack. The action is usually habitual, for example a man walks i nto a shop,
picks up something and walks out again, afterwards being arrested for
theft, or one who exposes himself in a public place and is arreste d for
140
indecent conduct; or a person cutting something may inflict incise d
wounds or kill a child; or a person accustomed to firearms may shoot
somebody.
• Twilight State : In this condition the field of consciousness is narrowed for
a short time, followed by amnesia. The patient may do some automat ic act
and is aggressive and suffers from visual hallucinations. It is usuall y in
epilepsy and rarely in hysteria, punch drunkenness and head injury.
• Psychomotor Epilepsy (temporal lobe, masked or psychic epilep sy) : In
this, instead of epileptic fit, the patient suffers from temporar y and
transient seizure of maniacal excitement with loss of conscious ness. The
patient may commit crimes without any motive.
The medico-legal psychiatrical examination of the epileptics m ust be done after they
are hospitalized in a psychiatrical section because a lot of te sts are necessary, including
EEG.
The judgment in epilepsy is absent only if the delict is commited during the epileptical
troubles (the attack, immediately after the attack, during the epi leptical aura) or if, after
many years of evolution, the patient presents “epileptogen state” characterized by:
epileptical character; paranoid psychosis; epileptical dementia.
12.3.3.2. Functional psychoses
Mental illnesses which have no neurological basis are called funct ional psychoses. The
functional psychoses are characterized by disorders of thought which have no physical
bases. In schizophrenic psychoses disorders of the thought process are dom inant. In
affective psychoses mood abnormality is dominant. This is a disease of hereditary
origin affecting young adults and forms a major group of all psychiatric ill nesses.
12.3.3.2.1. Schizophrenia :
It is a condition of split personality, in which the patient loses his contact with his
environment. It is primarily a disorder of thinking (cognition). This disor der can be in
form, stream, possession or content of thought. It is characterize d by splitting of
different psychic functions. Disorder of behavior : withdrawal from reality,
preoccupation with the self (narcissism), attribution of feeling of strangeness to outside
influence (depersonalization) and feelings that his mind and body are under control
(passivity of feeling). Disorder of thought : confused thoughts leading to thought
block, devious thinking leading to incoherence of speech often with newly formed
141
words. Disorders of affect : depression, elation, inappropriate moods, liability of mood,
anxiety and blunting of emotions. Delusions : of grandeur, paranoid, hypochondriac and
influence. Hallucinations : commonly auditory, sometimes visual and tactile.
Personality deterioration: affecting his work, family and social relationships. It is the
commonest type of insanity in homicidal crimes, especially where the victim is a
stranger. The impulses are not sudden and the crime is usually preced ed by much
complaining and planning.
• Simple Schizophrenia : Is begins in early adolescence. There is a gradual
loss of interest in the outside world from which he withdraws. There is an
all-round impairment of mental faculties. He becomes emotionally f lat and
apathetic and has difficulty in forming social relationships. He becomes
irritable and has conflicts about sex, particularly masturbation. C omplete
disintegration of the personality occurs later.
• Hebephrenia : It begins in adolescents or young adults. Thinking process is
disturbed. Wild delusions are present. Often conduct is impulsive and
senseless. Ultimately the whole personality may disintegrate complet ely.
• Catatonia : This is characterized by alternating stages of depressi on
excitement and stupor; impulsive suicidal or homicidal attacks and
auditory hallucinations are common. This phase lasts for few hours to f ew
days followed by a stage of stupor which begins with lack of intere st,
concentration and general indifference.
• Schizo-affective Psychosis : This is an atypical type of schizophrenia in
which there are mood disturbances. Attacks of elation or depression,
unmotivated range, anxiety, panic, occur.
Medico-legal aspects:
• He may enter in a catatonic phase of inactivity, which may chan ge into
violence;
• The social danger is considerable, as he lives in a hostile worl d of his own
and may use extreme violence in what he sees as self-defendance;
• The criminal aspects of schizophrenia include homicide, the most notorio us
multiple murders that make sensational international news stories;
• The felony may be the beginning of the disease, but it also may occur
during the evolution;
142
• The judgment is absent if the person is in a critical period of the disease –
schizophrenia have critical periods but also normal periods under the
medical treatment.
12.3.3.2.2. Paranoia (Pparaphrenia, Paranoid Schizophrenia) :
Paranoia is the mild form, and is common in males. Paranoid schizophreni a develops
insidiously in the fourth decade. It is characterized by suspiciousne ss, delusions of
persecution and auditory hallucinations. At first delusions are indefi nite, but later they
become fixed on some person. The patient usually retains his memory and orientation.
When delusions affect his behavior, he is often a source of danger to himself and
others. In paraphrenia, delusions and hallucinations are present, but the per sonality is
relatively intact.
Medico-legal aspects:
• The persons with paranoia commit a lot of delicts like: rapes, the fts, and
also murders.
• The judgment is absent during the delirium
12.3.3.2.3. Affective types (Maniac-depressive Psychosis):
Maniac – depressive psychosis shows wide swings of mood from euphoric elation to
deepest depression, quite out of proportion or often totally unrelated to ex ternal
circumstances. The two extremes of these moods are hyperacti ve, excitant at one and
depressive stupor at the other. The primary disturbance is of af fect. It occurs
periodically. This is a disease of hereditary origin affecting young adults, and forms a
major group of all psychiatric illnesses. Isolated attacks of ma nia and depression may
occurs in the same patient and some show attacks of one type only.
• Maniac phase: This is a condition of exaltation of the emotions and the
intellect. Acute mania: it is characterized by euphoria or irr itable mood,
excitement, loss of self-control, flight of ideas and great muscul ar activity.
Mood is elated, attention is fleeting and there is high degree of distraction.
Hypomania: it is the mildest from in which there is an exaggerat ed sense of
self-importance. Offences, such as petty theft, deception, indecent a ssault and
fraud may be committed.
• Depressive phase (melancholia): it is an intense feeling of depression and
misery without any cause. The sadness of mood is reflected in pos ture,
movements and facial expression. He retires from his usual socia l activities,
143
avoids friends. Suicide is well planned and is of great danger to the pa tient. He
may kill relatives, especially dependent young children. Homicida l and
suicidal tendencies co-exist. They have feelings of self-repr oach and guilt, and
marked psychomotor disturbances.
Medico-legal aspects:
a. In the depressive mood, the patient may commit suicide.
b. Even more dangerous, there is the possibility he may involve other mem bers of his
family in a murder-suicide episode.
c. In the maniac mode, the patient may commit sexual offences, the fts, blows,
murders, sometimes very violent.
d. The judgment is absent during the depressive and maniac mood.
12.4. Effect of alcohol or drugs on judgment
Generally, the effect of alcohol or any drugs on a person is no ex cuse for his criminal
actions. If the person voluntarily gets drunk or on drugs, then any subsequent criminal act
is his responsibility as he is supposed to be aware that drink or drug s have the potential of
affect his behavior. If the proves that these were not taken voluntari ly there is a possible
defense.
12.4.1. Pathological drunkenness
The judgment is absent in pathological drunkenness which is a very serious form of
alcoholic ingestion; in that conditions a person may commit a lot of delicts, even
murder.
Clinical aspects:
– After the person drinks a small quantity of alcohol (which has no effe ct on a
normal person), hallucinations, delirium, loosening of the sense of real ity and even
coma may appear. In these conditions, the person may commit suicide, blow s and
multiple murders.
– The phenomena are followed by a total amnesia.
– The pathological drunkenness appears on a pathological cerebral struc ture and in
individual peculiar conditions.
– The judgment is absent during the pathological drunkenness.
12.4.2. Chronic alcoholism
The chronic alcoholism changes the personality of the subject in different degrees
until severe delirium with hallucinations, delusions, dementia. A lot of felonies by all
144
means may be committed in that condition (thefts, sexual offences, rape, blows,
crimes).
The judgment is absent only if the psychical disorder is very seri ous (like dementia,
delirium)
12.5. Diagnosis of insanity
In typical case of insanity the diagnosis is easy, but in early stages, especially when he
has no permanent delusions, and in borderline cases, the correct diagnos is becomes
difficult. The object of the clinical examination is to form on opinion about the patient’s
mind and the degree of responsibility.
1. Preliminaries: note the name, age, sex, and address of person. Time of beginning
and end of each examination should be noted.
2. Family History: enquire into the mental condition of the patient’s parents and
siblings and whether any of them suffered from chorea, epilepsy, etc.
3. Personal History: a. history of previous mental disease in the pa rents. b. factors
connected with environment, such as parents and homes, over-protection as a
child, rejection, strictness, inferiority complex, discrimination by parents,
emotional maladjustments during childhood, emotional fixation during
adolescence to parents. c. psychogenic factors, such as repression, emotional
conflict and anxiety states. d. organic diseases, like cerebral vascular accidents,
head injury, acute fevers, advanced renal and cardiac disease, senile degenerative
condition, toxemias, etc. e. drug dependence to opium, pethidine, barbiturate s,
alcohol, cannabis, etc. f. domestic difficulties. g. emotional shock. h. f rustration in
life, love, sex, etc.
4. Physical Examination: a. observe the patient’s manner of dress ing and walking. b.
examine for the presence of deformities and malformations in the he ad or body. c.
note the pulse rate and body temperature, both of which may be incre ased. d. the
tongue may be furred. e. the skin is dry and wrinkled and the hands and fe et moist.
a complete and detailed physical examination should be carried out t o exclude any
disease.
5. Mental Condition: the following observations should be recorded. (1) General
appearance: naked, dressed properly, improperly, dirty of clean habits , and facial
expression, whether vacant, grimacing, masks-like or makes faces. (2) Talk:
mutism, aphonia, distraction, irrelevant, neologism (coining his own vocabular y),
145
echolalia (repeating identical words uttered by another person), per severation
(repetition of an act monotonously), wandering speech and talkative. (3) Speech:
coherent, incoherent, aphasia, lalling, lisping, drawling, slurring , stammering. (4)
Writing: agraphia, flight of ideas, obscene or insulting language, uninte lligible. (5)
Behavior: stereotypy, perseveration, mannerism, impulsive, lazy, stupor, autom atic
obedience, negativism, reclusive, echopraxia (copying all action of anot her) (6)
Mood: emotion, euphoria, joy, anger, elation, exaltation, apathy, irritable , touchy,
etc. (7) Memory: good bad, concentration, appreciation, grasp, etc. (8) S leep:
insomnia, hyposomnia, somnambulism, somnolentia. (9) Walking and gait:
stealthy, hurried, etc. (10) Attitude and posture: proud, peculiar, over-e rect,
aggressive, worried, etc. (11) Sex behavior: towards same sex and opposite, etc.
(12) Attention: attentive, fluctuating, inattentive, etc. (13) Thought pr ocess:
retardation, preoccupied, ambivalence, double orientation, power of orientat ion,
etc. (14) Thought content: delusions, hallucinations, illusions, obsession, sel f-
consciousness, etc.
6. Other Investigations: additional evidence can be collected from pathol ogical
examinations of the blood, urine and CSF, and X-ray and electroencephalog raphic
recordings.
Observation: the person should be kept under observation in a general hospital or
general nursing home, or psychiatric hospital or nursing home, or in any other suitable
place, which should not exceed ten days, but with the permission of the Magistrate, he may
be detained for further periods of ten days, up to a maximum of 30 days.
Violent and criminal persons should be kept in a prison. The person should be
watched during different times of the day, when he is alone, in compan y and while he is
working, eating, reading or writing, and when he is unwary of the fact of being obs erved.
146
CHAPTER 13: KILLING OR INJURY OF NEWBORN COMMITTED
BY MOTHER
13.1. Definition. Legislation
The problem of infanticide has been approached by different peoples in d ifferent
ways from ancient times. Similarly, in our country, laws have undergone modifications in
different historical phases. The Penal Code from 1864 stipulates that, “Infanticide means
the killing of children or newborn babies.” Penal law from 1936 states , “Infanticide is the
killing of a natural child by the mother before the expiration of the legal term of civil status
declaration (15 days from the child’s birth).”
The actual Romanian penal legislation comes from Article 200 – ”Killing or injury
of the newborn committed by the mother”:
(1) The killing of newborn immediately after birth, but no later than 24 hours, committed
by the mother being in the state of mental disorder shall be punished with imprisonment of
one to five years.
(2) If the facts set out in art. 193-195 are committed to the newborn i mmediately after
birth, but no later than 24 hours, the mother being at mental disorder, speci al limits of the
penalty shall be one month, respectively, 3 years.
The result therefore, like the crime, must include the following juridical eleme nts:
• Homicide can be produced by active action or negligence (commiss ion or
omission).
• The victim is a newborn baby.
• The action of killing is performed immediately after delivery, not later than 24
hours.
• The perpetrator of the crime must be the mother of the new born.
• The mother must present a mental disorder (Many known psycho-physiologi cal
abnormalities caused by delivery, which even without completely aboli shing
judgment can explain the abnormal conduct of women immediately after delivery)
Depending on the circumstances, the killing of newborn babies in conditions other than the
ones listed above can be classified as manslaughter or killing out of guilt.
Medico-legal expertise infanticide consists of:
• Examining the newborn’s cadaver.
147
• Examining the woman suspected of newborn’s killing.
• Examining the place of birth.
13.2. Medico-legal examination of the newborn’s cadaver
Medico-legal examination of the newborn’s cadaver must establish the following things:
1. The state of the newborn
2. Duration of intrauterine life
3. The newborn’s viability
4. Evidence of beginning extrauterine life
5. Duration of extrauterine life
6. Whether or not the newborn received necessary medical care imme diately after
birth
7. Cause of newborn’s death
13.2.1. The state of the newborn
The state of the newborn is established using:
Anthropometric parameters:
• The length of the newborn: At term, this is between 48 and 54 cm.
• The weight of the newborn: Usually, it’s between 2800 and 3500 grams.
• Cranium: this is relatively large, with a perimeter of 34-35 cm; the anterior
fontanel is rhomboid in form (about 2-2.5 cm x 3-3.5 cm) while the
posterior one is triangular, smaller, and open in 25% of newborns.
• Thorax: it is shaped like a cone, with the large base downwards, and a
perimeter of 31 cm.
• Abdomen: large, with a perimeter of 32-34 cm.
Morphologic characteristics:
• Traces of blood and vernix caseosa are present on the skin. Vernix caseosa
is a yellowish white fatty substance; in newborn at term, it can be found
either as thin layers on the thorax and abdomen, or as deposits behind the
ears, in the axillary and inguinal folds, and in the folds of the neck.
• The presence of serum-blood bossa: this is a gelatinous edema infil trated by
blood. Localized in the epicranian tissue, its margins are not circ umscribed
by the sutures.
• Skin: Incompletely developed both anatomically and functionally, it
contains a thin epidermis, no pigment, and is well-vascularized; this
148
explains the so-called newborn’s erythema, the redness in the fir st few days
after delivery.
• Placenta: this weighs 500-600 grams in an at-term delivery.
• The Umbilical cord measures 50-60 cm. In the first few hours aft er delivery,
it is turgescent and glossy, without a demarcating ring at the implantation
site. After 24 hours of supervision, a reddish-pink ring forms where t he cord
is attached to the abdomen, while the cord becomes more flaccid due t o
desiccation.
• Hair on the scalp measures 1-3 cm.
• The nails on the hands have gone beyond the digital pulp.
• Testes have descended into the scrotum.
• Labia major cover the labia minora.
• Meconium is found in the terminal intestine.
13.2.2. Duration of intra-uterine life
This can be appreciated using lunar or solar (calendar) months. A c alendar month
contains 30-31 days while a lunar one contains 28. A normal gestation l asts 10 lunar or
9 calendar months, a total of 280 days. Many parameters have been used to estimate
the duration of intra-uterine life. These include:
• Waist of the fetus: This parameter has the least variations. While a premature
newborn in the seventh month of intra-uterine life has a waist 36-38 c entimeters in
circumference, one at term has a waist of 48-54 cm.
• Weight of the fetus: This parameter has variations in very larg e limits. The weight
is about 1000-1400 g in the 7 th month of intra-uterine life, 1500-2400 g in the 8 th
month, and 2800-3500 g in the 9 th .
• Points of ossification: This parameter is very important in esta blishing the intra-
uterine age. According to Vipert, these points appear in the followin g order: at the
end of the 6 th month, the calcaneus (heel) begins to be outlined, at the astragal an d
sternum bones becoming well-contoured in the 7 th month. At the end of the 8 th
month, points of ossification are present in the sacral vertebrae. I n the 9 th month,
the point of ossification of the distal epiphysis of the femur (Bec lard’s nucleus) is
outlined, as is that of the proximal epiphysis of the tibia (Tapon’s nucleus), which
is better outlined and more constant. Points of ossification appear as ovoid reddish
149
gray zones 2.5 mm in diameter on the whitish-mother-of-pearl back ground of the
cartilage. These points resist advance putrefaction.
• Cranial diameter: In a fetus at term, these dimensions are 10.5-12 cm fronto-
occipitally, 8.5-10 cm biparietally, while the cicumference is about 35 cm.
However, in a premature of 7 months, these dimensions are 8-10.5 cm fronto –
occipitally, 6-8 cm biparietally, while the circumference is about 25 cm.
• Length of the umbilical cord: this varies from 40 cm in the 7 th month of intra-
uterine life until 50 cm in the 9 th month.
• Placental weight: this varies from 275-300 g in the 7 th month of intra-uterine life
until 500 g in the 9 th month.
13.2.3. Appreciating the viability of the fetus
Viability explains the fetus’s capacity to adapt to extra-ute rine conditions and
determines whether or not it can live autonomously in the new environme ntal
conditions.
The inferior limit of viability has decreased in obstetrics bec ause of better medical
care. Thus, according to WHO guidelines, in conditions of special me dical support, a
fetus in the 2 nd half of the 6 th month of intra-uterine and weighing over 1000 g is
considered viable.
However, medico-legal standards consider that only a fetus with a waist of 38 c m and a
weight more than 1400 g can be considered viable; these parameters cor respond to the
7th calendar month and a grade of prematurity that can allow surviva l without any
special medical assistance. From the medico-legal point of view , anything below this
limit can be considered an abortion.
On the other hand, a fetus can be considered non-viable when it presents congenital
malformation incompatible with life, is born with a severe infecti on contracted during
the intra-uterine period, or presents massive meningo-cerebral hemor rhages due to
obstetrical trauma.
Viability does not have any relevance in the juridical surroundings of the act, but in
some contexts it can provide extenuating circumstances to the killing mother.
13.2.4. Proof of installation of extra-uterine life
Proving that the fetus was born alive and lived after delivery, me aning the existence of
extra-uterine life, is the key element of medico-legal opinion. Wit hout this element,
there is no infraction (suppression of fetal life).
150
The best-known criteria that checks the installation of extra-ute rine life is the
appearance of pulmonary respiration, with the characteristic macro – and microscopic
modifications:
Macroscopic aspect of non-aerated lung : small lung, anrelaxed, occupying 1/3 of
the thoracic cavity, situated in the ribs-vertebral sinuses, with a smooth surface,
dark chocolate or intense red color, with a dense consistence on palpa tion, without
elasticity or crepitations. On section, it has the aspect of a pa renchymatous organ
and on pressure, a reddish liquid trickles out of it, without bubbles of air . Together,
both non-aerated lungs weigh 40 g in a fetus at term and 20-25 g in a premature
one in the 7 th month.
Macroscopic aspect of aerated lung : the lung is expanded and fills almost the
entire pleural cavity, its anterior margin surpassing the heart ; pinkish-white in
color, marble-like aspect, finely irregular surface with a pea rly shine given by
alveolar distension. The parenchyma is spongy, elastic, with crepi tations on
palpation but on section it spontaneously and/or on compression releases a pinkish-
red micro-aerated secretion that looks like foam. Together, both aera ted lungs
weigh 80 g in a fetus at term and 40-45 g in a premature one in the 7 th month.
Microscopic examination of the lungs is not sufficient from the me dico-legal point
of view for differential diagnosis. The Docimazy test, however, can differentiate
between aerated and non-aerated lung. Pulmonary Docimazy involves two
successive steps:
• Hydrostatic Docimazy: it is based on the difference of specif ic gravity
between the aerated/non-aerated lungs and the specific gravity of water.
Since water has a density of 1000, aerated lung, which has a dens ity of 450
– 800 floats in water while the non-aerated lung, which has a density of
1040, doesn’t. This test is valid only when the pulmonary tissue is not
altered by putrefaction. This test is carried out by throwing whol e pieces of
buco-cervico-thorax (cheek, neck, and chest) into a container of water. If
the piece floats, meaning the density of the lung is less than th at of water,
the lung is aerated. However, if the piece sinks to the bottom of t he
container, meaning its density is greater than that of water bec ause the
alveoli contain no air, the lung is non-aerated. In the next step of hydrostatic
docimazy, the two lungs are separated and introduced one after the othe r in
a container of water but the interpretation is performed in the same way.
151
Afterwards, fragments of the lung of various shapes and sizes (mm to cm)
from different areas are taken and introduced into the water. T hese
fragments may sink to the bottom, float at the water’s surface , or remain
somewhere between the surface and the bottom. Based on these results,
there might be non-aerated, aerated, or partially-aerated lungs.
o Partially-aerated lungs are seen in many pulmonary pathologies eg
interstitial pneumonia.
o In some situations, hydrostatic dozimetry may give incorrect res ults
as false positive or negative). Aerated lungs might present nega tive
docimazy (look non-aerated) in processes of condensation as in
pneumonia, in premature or immature atelectasis, and in atelectas is
secondary to air resorption. On the other hand, non-aerated lungs
might present a false positive docimazy (float like aerated lun gs) in
frozen cadavers, massive aspiration of vernix caseosa (float beca use
of fat contents), and in cases of putrefaction due to accumulation of
gases (after pricking the fragment, all gases will be rel eased and the
fragment will sink to the bottom).
• Pulmonary histo-pathological docimazy: this test is considered to have the
smallest indices of uncertainty or error. The preparations are first dyed with
hematoxylin-eosine, orceine (for elastic fibers), PAS (for pneumoni a with
hyaline membranes), and Scarlach (for fat).
o On microscopic examination, non-aerated lung has a compact aspect
with unrelaxed alveoli, like a slot with cubic alveolar cells w ith a
round nucleus; the bronchi have a small lumen with a folded
epithelium; the bronchiole have a stellate lumen, the bronchial
cartilages are away from the lumen, and the elastic fibers appear
undulated on orceine coloration.
o Aerated lung, however, shows expanded alveoli, with a
characteristic histopathologic aspect, polygonal spaces lined with
flattened and spindle-shaped alveolar cells with ovular nuclei; the
spaces are created by the thin dviding septae; the bronchi are
without folds, the bronchioli are relaxed, the peribronchial cartilage
is near the lumen, and the elastic fibers are straight, disposed i n
layers or semicircularly.
152
o Partially-aerated lung presents both aspects: areas of aerat ed lung
alternating with non-aerated.
o Putrefaction alters the histological structure of lungs, but thi s test
value is important in this situation, too. Thus, in case of aerated
lung, since microorganisms reach the depth by via respiration,
putrefaction bubbles appear first in the alveoli, breaking the alveolar
walls with artificially created emphysema with the involveme nt of
bronchioli and vessels. Elastic fibers resist putrefaction being
uniformly straight and diffuse in all pulmonary areas, even in
situations where the alveolo-capillary structure can’t be
distinguished anymore. In the non-aerated lung, putrefaction begins
at the surface and in peri-broncho-vascular spaces, and at the
lymphatic vessels, where the microbian flora is more abundant.
Elastic fibers are usually wavy, and their straightening due t o
bubbles of putrefaction is unequal with removal and
decentralization.
In the case of amniotic fluid aspiration, squamous polyhedral epitheli al cells,
basophilic and without nuclei, lanugo fibers without medullae, and fatty granules of sebum
(shown by Sudan III or Scarlach’s red) can be identified in the bronchi and alveoli.
Meconium is evacuated during prolonged intra-uterine hypoxia, and if m ixed with
amniotic liquid, can also be aspired; it contains mucus, epithelial c ells from the digestive
tract, rhomboid cholesterol crystals, and biliary pigment granules. M assive amniotic fluid
aspiration can produce death by asphyxiation and/or or giving rise to postnatal pne umonia.
Immersion in liquid, whether accidental or deliberate, leaves spe cific signs of the
immersion liquid. The microscopic exam shows the presence of patholog ic processes ie.
Interstitial pneumonia contracted during intra-uterine life, broncho-pneum onia, pneumonia
with hyaline membranes, etc.
• Gastro-intestinal docimazy (Besslau’s test) is another test that may prove
the existence of extra-uterine life. It can estimate the s urvival time in
minutes and/or hours after delivery. It proves the penetration of air in the
digestive tube after swallowing at the same time as its pene tration into the
lungs. A newborn who hasn’t taken its first breath has whitish flakes mixed
with a small quantity of viscous mucus in his stomach. Air penetrat es the
stomach after 5-10 minutes of extra-uterine life, the jejunal loops in another
153
15-20 minutes, and fills the entire small intestine in a maximum of 6 hours.
In the next 6 hours it penetrates the colon and in about 24 hours from
delivery, it can be found along the entire length of the colon.
• The digestive tube is extracted for docimazy after ligaturing the cardia,
pylorus, the small intestine before the ileo-cecal ampulla, and in the
terminal colon. The whole piece is submerged in a container of wat er;
pricking segments one after another can show which ones contain air. F or
correct interpretation of this test, the cadaver must not be in a state of
putrefaction.
13.2.5. Appreciating the duration of extra-uterine life
Since a newborn must be killed “in the first 24 hours after birth” for it to be
considered killing newborn committed by mother, survival after delive ry is divided into
two distinct groups:
1. Survival up to 24 hours
2. Survival more than 24 hours
13.2.5.1. Survival up to 24 hours
Survival up to 24 hours is determined based on:
The appearance of the newborn immediately after delivery: recog nized by skin
modifications; the skin is red in color as in an eruptive disease, s meared with
blood, and covered by vernix caseosa in the folds.
Finding umbilical cord modifications: after the interruption of feto -placental
circulation, the umbilical cord progresses through several stages:
• Immediately after birth, it presents a whitish-mother-of-pearl external
covering made of amnios, which constitutes the amnio-cutaneous line and is
continuous with the skin of the abdominal wall. Underneath the covering is
a layer of connective tissue comprised of a network of elastic fibers named
Wharton’s jelly. This jelly contains the three allantoid vesse ls, also
improperly named the umbilical vessels (two arteries and one vein). The
umbilical cord, with a thickness of 1.5-2 cm, has no lymphatic vessels.
• In the first 24 hours after death, examination of its amnio-cutaneous r ing is
very important because it estimates extra-uterine survival of a few hours
much better than the reddish demarcation ring, which can only be
macroscopically observed after 24 hours.
154
• Involution of the umbilical cord begins immediately after pulmonary
respiration and extra-uterine circulation. Thus, a process of aseptic necrosis
occurs at the amnio-cutaneous line, a groove appears which leads to the
sectioning of the umbilical arteries and vein and surrounding tissue, a nd the
umbilical stump falls off between the 5 th and 10 th days. Scarring of the
surface, followed by depression of this area, occurs from the peripher y
towards the center and finishes within 3-4 weeks.
Beslau’s test (gastro-intestinal docimazy), as shown above, can e stimate survival
time down to the minute within the first 24 hours after birth.
13.2.5.2. Survival more than 24 hours
Survival more than 24 hours is proven by:
Desquamation of the skin in small flaps begins 2-3 days after birth, and the skin
begins to regain its normal color of pinkish-white.
The presence of an amnio-cutaneous demarcation ring in the form of a red strip
denotes survival past 24 hours. Mummification and detachment of the umbil ical
cord ensue about 4-5 dyas after birth because the umbilical would heals in about 3
weeks.
Sero-sanguine bosses indicate survival up to 2-3 days; after this i nterval, they are
re-absorbed. These can be absent in prematures and in cases of induce d labor or
deliveries.
Complete elimination of meconium occurs in 2-3 days.
Botalo’s orifice closes in 2 weeks.
The ductus arteriosus closes completely in about 4-6 weeks.
13.2.6. Caring for the child after birth
Care of the child is important in cases of killing by omission. If the delivery is
unassisted, the woman may find it impossible to care further child ( involuntary
omission) or in other circumstances, or she purposely does not care f or the child
(voluntary omission).
In these situations, the following things must be examined at necropsy : the newborn’s
skin (whether it is washed or smeared with blood and vernix caseos a in the folds,
which denotes a lack of care), umbilical cord (whether it is se ction and ligatured or
torn and unligatured in omission), or if the respiratory orifices and p athways are
unobstructed. Afterwards, the stomach is examined with care. The absence of food in
155
the stomach and a urinary density more than 1012 prove that the mother did not feed
the child.
It must also be stated that a newborn’s resistance to thermal c onditions is very low.
Hypothermia at 32 degrees Celsius for a period of 24 hours can be f atal for a newborn,
so not wrapping the baby even in a warmer season can be fatal and denot es a lack of
care. It is still difficult to prove that a child died from the cold at autopsy. Conclusions
in such cases are reached by corroborating all the circumstances.
13.2.7. Causes of death of the newborn
Death of the fetus can occur before, during, or after birth.
13.2.7.1. Fetal death before delivery
Fetal death before delivery can be:
Due to pathologic causes by:
• Maternal diseases: following a febrile disease, cardiopathy, hep atic or renal
diseases, diabetes, tuberculosis, syphilis, tumors of internal genital organs,
Rh incompatibility, tardive dysgravidias, etc.
• Fetal diseases: following congenital malformations incompatible with
survival, intrauterine infections, hemolytic diseases, etc
• Placental diseases: following its infarct, placenta previa, abrupt io placenta,
premature placental detachment, etc.
Due to violence:
• Maternal trauma during the last part of the pregnancy, after the 7 th month,
especially localized in the abdominal area. These injuries might be
intentional or may occur during traffic, work, or household accidents.
• Accidental intoxications, maternal poisoning.
• Physical factors acting upon the mother: hyperthermia due to prolon ged sun
exposure, leading to a state of thermic shock; burns from boiling liquids or
open flame can cause intra-uterine fetal death, even if the mother survives.
• Voluntary intra-amniotic injection of chemical substances e.g. for mol or
hypertonic liquids with sodium chloride and/or glucose cause violent intra –
uterine fetal death. A violent intra-uterine death is declared onl y in
extremely objective situations where the causality cannot be conte sted.
From the juridical point of view, violent fetal death in the 7 th -9ths months
of intra-uterine life, regardless of whether it occurs intentional ly or
156
accidentally, does not receive special consideration because it i s similar to
the interruption of pregnancy.
13.2.7.2. Fetal death during delivery
Fetal death during delivery can be:
A. Due to pathological causes : following prolonged fetal hypoxic processes
during delivery, which can have many causes:
• Pathological states of the umbilical cord: long cord more than 60-65 c m,
cord circulation, intramural hematomas of the umbilical cord, short co rd
less than 30 cm, varices of the umbilical cord.
• Pathological processes of the placenta: placenta previa, placenta previa,
premature detachment of the placenta
• Maternal dystocia (mechanic or dynamic uterine casues): pelvi c
abnormalities, osteomalacia, pelvic or coxo-femoral joint deformations ,
fibromas causing uterine contraction abnormalities, uterine or neighbor ing
tumors, uterine or vaginal malformations, rigidity of the cervix, etc.
• Fetal dystocia: large fetus, hydrocephaly, fetal edema, fetal tumors .
• Congenital diseases, cardiac malformations, respiratory anomalies ,
hereditary enzymatic anomalies, malformation or immaturity of the central
nervous system.
• Regardless of the cause, both intra-uterine and intra-natal asphy xia lead to
petechia and gelatinous edema in the loose connective tissue.
B. Secondary to obstetrical trauma : appear frequently in practice and have a
great medico-legal importance because these lesions can be confuse d with those
produced during killing newborn committed by mother or may draw attent ion to a
lack of assitance during delivery. Obstetrical trauma of newborns can be classified
based on the types of lesions in three main categories:
• Cranio-cerebral and peripheral nervous system lesions: sero-sangui nous
bosses, external cephal-hematoma, epidural hematoma (internal cepha l-
hematoma), cranial vessel lesions, subdural hemorrhage, cerebellar cortex
rupture with supra- and infra- tentorial hemorrhage, intra-cerebral
hemorrhage, brachial plexus rupture, etc.
157
• Osteo-muscular system lesions: sterno-cleido-mastoid rupture or
hemorrhage, first rib fracture, clavicular fracture, dislocation of the
humeral, tibial, or femoral epiphysis, long bones’ fractures.
• Lesions of internal organs: hepatic subcapsular hematomas, spleen ruptur e,
supra-renal hematoma.
Obstetrical injuries can be produced by the following mechanisms:
Compression of the head while traversing the pelvi-genital tract.
Obstetrical instrument intervention to extract the newborn (forceps delivery,
internal version).
Auto –assisting delivery.
Accidental, in induced labor or during resuscitation.
From all the above-mentioned lesions, cranio-cerebral lesions produced by obstetrical
trauma are easiest to confuse with those of violence produced during kil ling newborn
committed by mother. The main cranio-cerebral lesions seen in obstetrical t rauma are:
• Cephal-hematoma: blood situated sub-periosteally, secondary to compress ion
and traction on the small and deep vessels. It is well delimited b y the sutures
and does not pass their edge. Most often situated parietally. Evolve s
spontaneously to re-absorption in 4-6 weeks. Sometimes it can even cal cify and
ossify.
• Sero-sanguinous bosses: appear in prolonged labor due to differences in
pressure. Sero-sanguinolent edema occurs in the epicranian tissue at the site of
minimum pressure over the entire site exposed to suction. This lies over more
bones but it reabsorbs in 24-48 hours.
• Cranial fractures: these are known as Potter’s fractures, whi ch are linear,
regular, uneven, situated on the top of the head, and rarely irradiating.
• Meningo-vascular lesions: these are the most important obstetric al trauma
lesions, often present even in the absence of cranial lesions.
Thus, scythe brain and cerebellar cortex show limited resistance to the deformation of
the cranium, giving rise to lesions usually localized in the areas of junction, with the
appearance of lacerations of the thick meninges, lesions of the scy the brain with tears
of the longitudinal sinus and intra-cranial hemorrhage. Subarachnoid hemorrhag es are
frequent and stretched as the surface surpasses the cranial lesions.
158
An important characteristic of obstetrical cerebral hemorrhages, regardless of
localization, is the bilaterality of lesions with predominance on the part of pres entation:
• Cerebral lesions: the brain is relatively malleable, and modifi cations of volume
and form are reversible.
o Frequently, one finds petechial hemorrhages in the structure of th e
nervous system similar to the ones in diffuse cerebral contusion, whic h
also include repoured intra-parenchymatous blood that usually is
localized in a single hemisphere.
o Repoured intraventricular blood, relatively frequent in the field of
obstetrical trauma, is associated as a rule with other trauma tic lesions. It
is given by ependymal lesions.
• Vertebral column lesions of obstetrical origin have been found even in
deliveries where it seems that there was no unusual mechanical solicitation,
which includes even those via autoassistance. The main lesion in t his category
is intra-spinal hemorrhage.
C. Secondary to auto-assistance: it is possible while lesions of violence found on
the body of the fetus must be differentiated from those that may be produced
during killing newborn committed by mother. Lesions characteristic for auto-
assisted births are:
• Excoriating lines, nail- or crescent- shaped with their concavit y pointing
upwards situated on the hairy skin of the head, forehead, face, palatine vault
(concavity oriented anteriorly), and the inferior surface of the m andibular
region.
• Oval ecchymoses 1-1.5 cm, majority of which are demarcated b y the
excoriating lines mentioned above.
• Ruptured wounds which start from the buccal commissure and go upwards.
• Depression of an eyeball due to digital pressure.
• Fracture of the mandible in its medial portion, with the superior proje ction of
one ramus, and damage of the soft tissues normally anchored by the mandible.
• Biparietal fracture looking like “two V’s” oriented transversall y (horizontally)
with the lateral margin and opening on to the sagittal suture. This type of
fracture occurs during auto-assistance when one tries to releas e the cephalic
extremity from below upwards, transforming the presentation into to a
159
deflected face, which by holding the mandible and performing avulsi on
maneuvers fractures the mandible, presses the two parietal bones on the inferior
margin of the pubis, and produces the above mentioned fracture.
13.2.7.3. Death of the fetus after delivery can be:
A. Of pathologic cause : the most frequent causes of pathologic death in the
perinatal period are:
• Malformations that are congenital, severe, and incompatible with l ife, such
as:
o Monstrous anencephaly, cyclopia, spina bifida, rahiskizis;
o Severe cardiac malformations: ventricular septal defect (Roge r’s
disease), defects of atrial trunk division (common trunk of the large
vessels), Fallots triad or tetralogy, coronary artery anomalies, etc.
o Malformations of the respiratory apparatus: imperforated nostril s,
mandibular hypoplasia, macroglossus, epiglottic cysts, lryngeal
stenosis, tracheal compression due to abnormal positions of the
large vessels, unilateral pulmonary agenesis, etc.
o Severe malformations of the digestive system: tracheo-esophageal
fistula, diaphragmatic hernia, umbilical exomphalos with
involvement of the liver, esophageal atrexia and stenosis, intestinal
atresia or occlusion, etc.
• Materno-fetal blood incompatibility by isoimmunization: Rh
incompatibility causes severe jaundice of the newborn with anemia, ye llow
coloration of the red nuclei at the base of the brain, hepato-splenomegal y,
feto-placental anasarca, and edema.
• Hemorrhagic syndrome of the newborn occurs during day 2-5 post-
delivery. It is characterized by cerebral, epicardiac, diges tive pulmonary,
suprarenal, and cutaneous hemorrhages.
• Pneumonias and bronchopneumonias may begin during the intra-uterine
period.
• Hypertoxic hemorrhagic viral diseases can cause meningo-encepha litis,
interstitial myocarditis, and interstitial pneumonia with an acut e evolution
and death in 24-48 hours.
• Hyaline membrane pneumonia.
160
• Umbilical infections, triggered during the intra-partum period by i nfected
amniotic liquid or vaginal contamination, or post-partum with germs fr om
the external environment, which eventually lead to death via septicemia.
• Immaturity
• Other causes of death may be massive amniotic liquid aspiration, pri mary
pulmonary atelectasis, and last but not least, the “syndrome of unex plained
death of the newborn,” a situation in which medico-legal autopsy cannot
macro- and microscopically describe characteristic elements f or a specific
disease or cause of death but only non-specific anatomo-pathological
modifications such as generalized edema, stasis, and some subpleura l
petechiae.
B. Of violent causes :
• Produced accidentally due to many causes:
o Accidental trauma, which can appear in the following conditions:
Induced birth, after a relatively short labor, with quick
expulsion of the fetus in the woman in the standing position,
leading to falling of the fetus.
Qualified or even unqualified assistants at delivery, where
the newborn falls from their hands due to a fatty protective
layer on their skins, with the appearance of unipolar lesions,
fissures, or fractures on the point of impact.
o Accidental asphyxiation: can be found in induced deliveries where
the fetus falls into the toilet or into a basin with liquid.
o Hemorrhagic accidents: can appear in all induced deliveries, where
the woman is standing up, by stretching and tearing of the umbilical
cord from its point of insertion before pulmonary respiration has
begun.
o Accidental intoxications: appear due to a habit of giving the mother
alcohol during the delivery to decrease pain.
• Produced during infanticide or homicide.
13.3. Methods of killing the newborn by his mother
The infraction of killed can be committed by:
161
• Action or direct intention
• Inaction or indirect intention, meaning in a passive manner by not fulf illing the
obligations or providing a newborn with the care necessary for survival.
In general in medico-legal practice, active and passive killing is used to classify the
infraction from the point of view of medico-legal tests.
13.3.1. Active killing
This is committed by a violent action such as the methods of asphyx iation, traumatic
aggression, physical means (e.g. exposure to cold) and/or chemical (e.g. intoxicat ions).
13.3.1.1. Asphyxia
Asphyxia represents the main method used for killing.
The types of asphyxia are listed according to frequency:
Suffocation:
• is performed most frequently by putting a soft object on the newborn’s face,
such as a pillow, blanket, towel, handkerchief, nylon sheet, etc. In the
majority of cases, no traces of violence are left, and autopsy only finds
general signs of anoxia which further necessitate confirmation b y histo-
pathological exam.
• In other situation, suffocation is performed by introducing a foreign body
into the mouth or pharynx. These can be diapers, clothes, cotton, paper, etc.
and they will be found whole or in fragments in the oropharynx. Often in
these cases signs of violence are also found in the form of bruises,
excoriations, and mucosal erosions, which must be investigated by
sectioning on autopsy to find the vital character. The lips may fr equently
become parchment-like due to dehydration.
• Accidental suffocation by compression against the mother’s breast points to
imprudence in the newborn’s care.
• Suffocation by putting the newborn in a space without air such as a pl astic
bag, refrigerator, or perfectly-closing suitcase is another for m of killing the
newborn by his mother where autopsy finds no signs of violence, only
general signs of anoxic anoxia.
Strangulation can be performed using a soft material, such as a scarf,
handkerchief, or kerchief –when the external examination of the cadaver does not
show signs of violent or grooves or strangulation—or hard or semi- hard materials,
162
such as a wire, belt, or shoelace—when a typical groove of strang ulation is evident
and parchment-like, which macro- and especially microscopically has a vital
character (meaning it was created while the child was still alive).
Suppression or strangulating the baby with one’s bare hands leaves
characteristic signs on the neck: bruises and lenticular excoriat ions oriented
vertically and/or oblique on the anterior surface of the throat. These lesions must be
differentiated from those of auto-assisted delivery.
Drowning the newborn in a well, running water, latrine, or container of water a re
all time-tested methods. In latrines with thick contents, the newborn’ s body
remains on the surface and he asphyxiates due to mephitic gases. In latrines with
liquid contents, asphyxia is produced by aspiration of fecal matter, which will be
found the respiratory tree and stomach on autopsy. Pushing the newborn into t he
toilet bowl during infanticide produces traumatic lesions such as ecc hymoses and
excoriations on any prominent parts. These may even include circul ar cranial
fractures. Drowning the newborn in a container of water mixed with cleaning l iquid
leads to aspiration of blood, meconium, and elements of the immersion liqui d. In
case of drowning in running water or lakes, plankton will be found on microscopic
exam. Asphyxia by drowning in these cases by drowning is proved to be vital if
diatoms are found in the kidneys and bone marrow.
13.3.1.2. Traumatic aggression
Traumatic aggression has the same frequency as asphyxia as a cause of killing the
newborn by his mother, but it can objectively differentiated from o bstetrical trauma,
whether accidental or by auto-assistance. Repeated blows of the ce phalic extremity
with a blunt object are frequently seen. Lesions are multipolar, wi th hematomas in
many areas of the head and comminutive fractures that interse ct sequentially and
involve multiple bones. Osseos lesions are always accompanied by me ningeal
hemorrhages.
Rarely, cranio-cerebral lesions are produced by grabbing the infant by the feet and
swinging the cephalic extremity into a hard surface. In this s ituation, a very tense
meridional fracture appears.
killing the newborn by his mother using cutting or pricking instruments is also seen
relatively frequently. Sectioning the organs of the throat, stabbing the thoracic cavi ty in
the precordial area, and/or opening the abdomen, and decapitation are all described in
specialist literature.
163
Combined traumatic aggression is often seen, e.g. Hitting the cephalic extremity with
or against a hard object followed by twisting the organs of the neck.
13.3.1.3. Killing the newborn by his mother through the action of physical factors ,
seen more rarely, by burning or scarding the new-born requires deter mination of the
vital character.
13.3.1.4. Killing the newborn by his mother through he action of chemical factors
Infanticide by the action of chemical factors such as poisoning b y caustic soda or even
a modern toxin, is rarely seen in practice.
13.3.2. Passive killing
Rarer than active killing, passive killing is also more difficult to prove in criminal
investigation. It refers to intentionally not fulfilling the obligat ions of providing
necessary medical care to the newborn; examples include not cutting the umbilical
cord, not wrapping the baby, and abandoning him or her in inadequate environme ntal
conditions.
As mentioned above, exposing the newborn to a temperature of 32 degrees Cel sius for
a period of 24 hours leads to death. In these situations, it is necessary to corroborate the
investigations about the duration of the exposure to low temperatures wi th the medico-
legal observations on the duration of extra-uterine life.
A mother’s involuntary omission to provide care to the newborn is anothe r situation by
killing newborn by his mother which may or may not be perceived objectively.
Appreciating the level of intention or motivation for providing neces sary care to the
newborn is not the job of the medico-legal expert. Their task is to describe objective
findings from the fetal cadaver and the state of the mother after delivery.
Extremely advanced putrefactions of the newborn can sometimes make i t impossible to
pinpoint the cause of death and therefore the type of killing newborn by his mother, a
fact which must be mentioned in medico-legal evaluation.
13.4. Medico-legal expertise in cases presumed to be killing newborn by h is mother.
This is performed to establish the signs of birth, when the mother is not unknown,
and/or finding disturbances related to the delivery when the mother is known.
Sometimes, the woman suspected of killing newborn is found in a short p eriod of
time, since the signs of recent delivery are found. However, other t imes, the examination
of women is performed after a longer period of time, finding only signs of multiparit y.
164
The examination of women includes a general clinical examination, a
gynecological exam, and laboratory investigations to find signs of a recent delivery and the
period of delivery, after which a detailed psychiatric examination is performed to find any
psychiatric disturbances caused by the delivery.
The diagnosis of a recent delivery is based on:
• Uterine involution: in the first day after a delivery at term, t he uterus can be
palpated at the umbilicus, after which it descends about two fingers per day, and
thus in the 5 th day it is situated at half the distance between the umbilicus and pubis
while 6-8 weeks after delivery it reaches the superior margin of the pubis.
• Aspect of the lohyes: these are bloody in the first week aft er delivery, after which
they become sero-mucous or yellow-white, a sign that they have flowed for 2
weeks.
• Colostrum secretion: present in the first days after delivery, c olostrum will
coagulate upon boiling due to the high content in proteins.
• Lactation secretion starts 3-4 days after a delivery at ter m. Drops of maternal milk
become red after a combining with Scharlach’s reactant, which confi rms that a
delivery occurred at term about 4 days ago.
• Aspect of the genital organs: after a recent delivery, one may find vulvae edema,
perineal fissures, perineal ruptures of any grade, and ruptures of the vaginal wall or
cervix, all with blood-infiltrated margins and a recent aspect.
Since an act may or may not be considered killing newborn, there ar e many signs
in the post-partum period and lab investigations that can show secondary e ffects of
obstetrical complications such as sever hemorrhoids with severe sec ondary anemia, toxico-
septic state, etc, proving the impossibility of providing adequate me dical care to the
newborn immediately after delivery (involuntary omission), a situati on which does not
involve punishment.
Maternal death after delivery terminates penal action for the crime of killing
newborn. However, in cases of hetero-assistance (qualified or unqualifi ed personnel),
medico-legal investigation in the case of maternal death after deliver y places guilt upon the
persons who assisted the delivery; these may also be charged as accessories to the murder
of the newborn.
In case the woman is examined after a long period of time, a pre vious vaginal
delivery can be proven by finding a transverse slot of the external orifice of the cervix, the
165
presence of scars after perineal rupture, and perhaps stretch ma rks on the abdominal wall.
All these elements are difficult to prove because of their age.
Psychiatric and psychological examination, as mentioned earlier, m ay find the
presence of psychiatric disturbances caused by delivery in a mother accused of killing
newborn. These exams have primary importance in legal consideration of the act;
however, retrospectively, it is very difficult to estimate the discernment, especially from
the time of delivery. Proving the abolition of judgment due to a psychi atric illness (usually
lactation psychosis) will absolve the woman of legal responsibility . However, if it is
proven that the mother possessed adequate judgment and the act was pre meditated
prenatally, she is considered a murderer. If judgment was proved to be diminished as a
consequence of the delivery, it might still be considered an infraction of killing new -born.
Disturbances that appear immediately after delivery can have causes other than
psychiatric and various intensities. Some examples of disturbances pr ecipitated by delivery
include psycho-emotional disturbances, hemorrhages from the moment of bir th, obstetrical
shock, etc.
The sooner the woman is examined after delivery, the better a di sturbance caused
by delivery can be diagnosed. As time passes, legal consideration of the act becomes
progressively more difficult.
The woman’s behavior can be checked only by combining many elements , such as
researching the previous medical history, prenatal conduct, persona lity, psycho-
pathological tendencies during stress (e.g. delivery), evolution of the pregnancy,
conditions in which the birth occurred, social environment of the woman (a nd higher level
of culture and civilization decreases the incidence of cases of killing newborn by his
mother, according to specialist literature), pre-existing conflicts, et c.
13.5. Examination of the place of delivery
This is a compulsory step in investigating killing newborn because i t adds
information regarding how exactly the birth took place. The place might present signs of
delivery, such as a placenta, traces of blood, amnios, objects used duri ng delivery (clothes,
sponges), and objects pertaining to parturition; all these elements a re tests used during the
investigation, especially in identifying the woman.
The place of birth can also indicate, as stated above, the conditions in which it was
carried out: isolated places, induced delivery, large hemorrhages, etc and other elements of
great importance in a criminal investigation.
166
CHAPTER 14: SEXUAL OFFENCES
14.1. Classification:
I. Natural offences:
• Rape;
• Incest.
II. Unnatural offences:
• Sodomy;
• Tribadism;
• Bestiality;
• Buccal coitus.
III. Sexual perversions:
• Sadism;
• Masochism;
• Necrophilia;
• Fetichism;
• Transvestism;
• Exhibitionism;
• Masturbation;
• Voyeurism;
• Frotteurism;
• Undinism.
14.2. Natural offences
14.2.1. Rape
Definition: Rape is the offence according to the 218 C.P. article. “Intercourse, or al
or anal intercourse with a person committed under coercion implementi ng unable to
defend or to express the will or taking advantage of the same conditi on, shall be punished
with imprisonment from 3 to 10 years and deprivation of some rights”.
Most rapes are committed by men, victims being females. A ma n is said to commit
rape, if he has sexual intercourse with a woman:
– against her will,
– without her consent,
167
– with her consent when her consent has been obtained by putting her on a ny
person in whom she is interested in fear of death, or of hurt,
– with her consent, when the man knows that he is not her husband and tha t she has
given consent because she believes that he is another man to whom s he is lawfully
married,
– with her consent, when at the time of giving such consent, by reas on of
unsoundness of mind or intoxication or the administration of any stupefying substance, she
is unable to understand the nature and consequences of that to which she gives consent,
– with or without her consent, when she is under 16 years of age.
Exception: sexual intercourse by a man with his own wife (even against her will) is
not rape, if she is above fifteen years of age.
Consent: a woman of sixteen years and above can give valid consent for sexual
intercourse. The consent must be free and voluntary, and given while she is of sound mind
and not intoxicated. The consent should be obtained prior to the act. Even a prostitute
cannot be forced to have intercourse against her will.
Consent is not valid:
• When it is obtained by fraud, as by impersonation of the husband or by
misrepresentation of facts,
• When it is obtained by putting her or any person in whom she is inter ested,
in fear of death or hurt,
• When obtained from a woman who is of unsound mind, or who is
insensible, or is asleep, or is in a state of semi-consciousness or in a state of
drunkenness,
• When the woman is below sixteen years of age.
Presumption and Proof of Consent: consent or its absence can be presume d from
the accompanying circumstances of each case. The chief evidence of lack of consent is
signs of resistance, which is naturally expected from a woman unwilling to a sexual
intercourse forced upon her. Such a resistance may cause the teari ng of clothes, and
injuries on the body, and even on her private parts. It is necessar y to prove that maximum
resistance was offered by the woman, ant that all mans had been t ried to prevent sexual
intercourse (example – shouting, crying, beating, biting. The woman may surrender from
fear or exhaustion, in which case it is regarded as rape. Woman who faint due fear, or are
made helpless due to their clothes being thrown on their face, or who have been drugged or
168
unconscious from any cause, and children may not be able to resist. The resistance offered
depends upon the type of woman, her age, development and on the social status . In most
cases of rape physical injury involves hitting or slapping the victi m, chocking her,
knocking her to the ground, and/or forcibly tearing her clothes. Even though t he rapist may
not employ physical methods or a visible weapon in his track, the vi ctim is convinced she
is in mortal danger and reacts by doing whatever appears most li kely to preserve her life.
Often this involves non-violent submission to her assailant.
What Constitute Rape? – The slightest penetration of the penis wi thin the vulva,
such as the minimal passage of gland between the labia with or wit hout emission of semen
or rupture of hymen constitutes rape. There need not be a completed a ct of intercourse. It
is an essential part of proof in a rape, that there should have been not only an assault but
actual penetration. Rape can be committed even when there is inabili ty to produce a penile
erection. Rape can occur without causing any injury, and as such nega tive evidence does
not exclude rape. The doctor should mention only the negative facts, but should not give
his opinion that rape has not been committed. Corroboration by eye witness es or
circumstantial evidence is necessary in such cases.
Exception: a husband cannot be guilty of rape on his wife, if she is a bove fifteen
years, because in marriage the wife consents to the husband’s exer cising the marital right
of intercourse during the continuation of legal marriage.
Under the law, rape can only committed by a man and a woman cannot ra pe a man,
although she may be guilty of an indecent assault upon him.
In Romanian Penal Code (art. 219) punished the man who had sexual reports with a
woman through physical or psychical coercion or with a woman who cannot protect
herself (example – woman in coma, with neurological diseases) or who cannot express
their will (example – woman with psychiatrically diseases).
In order to distinguish the rape, the forensic pathologist must exa mine two
essentials aspects:
• The signs of a sexual report (the victim of rape may be virgin w omen or a
sexual active women);
• The lack of agreement from the victim
169
CLINICAL EXAMINATION IN CASE OF RAPE
Is examined usually the victim and sometimes (when requested by the police) and the
aggressor is examined too.
A. Examination of the victim includes:
1- somatic exam to establish the presence of the violence lesions;
2- psychiatric exam;
3- blood test for the establishment of the presence of the alcohol – if it is
considered;
4- gynecological exam;
5- culture of the vaginal secretions;
1. – presence of the violence lesions is probing the non-agreement of the victim. In these
cases lesions more often found are on the face, neck, lower member s (iliac region) and
around the external genital organs.
In case of the bite wounds is taken the dental print.
Also, on the body and the underwear of the victim is looked for hair, b lood stains and
sperm belonging to the aggressor.
The clothes may be reaped off as a sign of struggle with the aggressor.
2. – Is establishing if the victim may express free will a nd consent and if it able to
appreciate the consequences of the sexual act;
3. – Genital exam:
– Is done in the presence of the third person for avoiding of any eventua l tendentious
affirmation from the examined person (e.g.: that defloration occurred during the exam)
– Is followed after a short history about what happened (with atte ntion to any blackmail
tendencies or some fantasy remarks);
– Examination is done on the gynecologic table in the Trendelenburg position;
-The examiner moderately tracts the labia majora with the hel p of two sterile pence
anteriorly, laterally and eventually up;
– After the examination with the free eye is done a stereoscopi c exam through which the
image is enhanced by 12 times;
Is examined the hymen: which is a mucous ply, circular situated a t the limit of the
vulva and inferior part of the vagina.
Description presents:
• a base – through it enters the vagina;
170
• free margin – which delimits the hymen orifice;
• superior part (oriented to the vagina)
• inferior part (downward, visible at the examination)
The hymen may have more shapes which are individual and more exactl y: ring form (with
a central orifice); half moon like (wider in the inferior part w ith the excentric orifice),
bilabial (formed from two valves united anteriorly and posteriorly by a comissure);
rudimentary (very narrow, permit easy dilation, permits sexual act without being injured),
lobe like (is formed from more segments). In case of defloration i njuries present small
differences depending on the hymen shape.
As consistency is described:
– non-dilation hymens with fibrous, tendon like structure which are broken ve ry
hard;
– dilation hymens with elastic, lax structure in which the first sexual contact doesn’t
produce any bleeding or any pain and the real defloration is produce d at the first
delivery.
Free margin of the hymen is pink, uniformly thick, smooth and rarely shaped with shallow
spots of different depths. It is delimiting the orifice of the h ymen which is round or oval
with diameters of 1-1.5 cm after the puberty (is smaller in girls).
Exists and cribriform hymens (with many orifices) or non-per forated hymens.
Width of the hymen is the distance between the free margin of the hymen and its base.
Depends on the shape of the hymen (0.5 in ring like hymens, smaller in the rudimentary
one, 1.5 in that half moon shaped).
In case of rape during 7-8 days from defloration the hymen presents injuries:
– in variable number (2,3,4)
– incomplete or complete (if they rich or not the base of insertion of the hymen
membrane)
– sometimes may imply and vaginal mucosa or vulva.
These injuries have margins: red, bleeding, tumefied, covered with fibrin for a
period of 5-8 days. More rarely are found echymoses or hematomas in the areas of injures.
This aspect represents the recent defloration.
After 7-8 days after defloration begins the process of scaring. Margins of the
ruptures are thinner, are retracting are white-red and the white-pearl.
171
In 10-14 days after defloration the injuries may be seen just in stereoscopic exam.
After this period all the signs of defloration are absent.
In case of old defloration often appears the situation to differentia te old ruptures of
congenital incisures (difficult work). But mainly, congenital incisures are characterized by:
symmetrical disposition, are incomplete, don’t have scaring tiss ue, have well delimited
margins.
4. – Culture is done with a stick from the bottom of the vaginal base.
Microscopical exam reveals the presence of the spermatozoids in vaginal sec retions
in the period of 1-2 days from end of the sexual act if in this time the woman didn’t get
any bath.
It is observed spermatozoids or fragments of it. Number of the exa m id is written in the
observation nr 1.
B. Examination of the aggressor
– looks for the revealing of violence lesions, psychiatric state, event ually consumption of
alcohol, presence of the hair (is compared with the victim hair or with the one present on
its head), any blood trails (blood group – is it as victim’s?) or spe rm on the body or
clothes.
C. Conclusions:
– reality (or not) of the sexual act (recent or old)
– presence of the violence lesions on the body
– impossibility (eventually) psychiatric or physical of the vict im to express the free
will or to defend.
In the absence of recent local lesions the virginity is certain, more delicate issue is
the presence of elastic and dilation hymens (permits sexual act without the
defloration)
It is the possibility of defloration without the rape, through digital man operas
(incomplete ruptured hymens, abrasions at the level of vulvar and vaginal mucosa).
Dangers of Rape:
Sometimes the victim is death. Death may occurs from:
– Shock due to fright and emotion or by blunt force,
– Haemorrhage from injuries to genitals and perineum
– Suffocation if mouth and nostrils are closed by the hand or cloth or b y
strangulation.
172
In this case the punished is more to 7 years (between 7 and 15 years).
Sometimes the victim presents mental derangement, convulsions and epi leptic fits.
Psychological trauma is much more when the victim knows the rapist.
It may disrupt the victim’s physical, social and sexual life.
Rape on Children :
In young children there are few or no signs of general violence , for the child
usually has no idea of what is happening, and also incapable of resisti ng. The hymen is
deeply situated, and as the vagina is very small, it is impossible for the penetration of the
adult organ to take place. Usually, the penis is placed either withi n the vulva or between
the thighs. As such, the hymen is usually intact and there may be l ittle redness and
tenderness of the vulva.
As the penis enters the genitals, it tends to compress the labia bot h anteriorly and
laterally, producing bruising of both the labia minora and the labia ma jora. The amount of
bruising will depend upon the force used. Further penetration forces the p enis backwards,
because the symphysis pubis prevents anterior movement, and the hymen i s torn
posteriorly. As the penis advances into the vagina, additional pressure is put on the anterior
and lateral structures and the hymenal tear extends into or throu gh the perineal body and
often involves the anterior wall of the anorectal canal. The younger the child, the more
widespread are the injuries. Circumferential tears of the mucosa of the vestibule are
common. As the age and size of the infant increases, the patter n f injury will become less
marked but the circumferential tears of the vestibular mucosa are found up to the a ge of six
years or more. Full penile penetration produces bruising of the vaginal w alls and
frequently tears of the anterior and posterior vaginal wall. Anteri or tears can involve the
bladder and the posterior tears the anorectal canal. Vaginal v ault may rupture, and there
may be vaginal herniation of abdominal viscera. The hymen may be entirely destroyed or
may show laceration. Blood may be oozing from the injured parts, or clot s of blood may
be found in the vagina. There may be mucopurulent discharge from the vag ina. In digital
penetration of the infant vagina, there is frequently some scratchi ng or bruising of the labia
and vestibule, but the circumferential tears are absent. The hymen shows a linear tear in
the posterior or posterolateral quadrant, which may extend into the post erior vaginal wall
and on to the skin of the perineum, and may involve the perineal body. Ano-rec tal canal is
rarely involved. Bruising in the margins of tear and of anterior vagi nal wall are common,
but vaginal vault injury is rare. Any attempt to separate the thi ghs for examination caused
173
great pain, because of the local inflammation. The child walks wit h difficulty due to pain.
The absence of marks of violence on the genitals of the child, when an ea rly examination
is made is strong evidence that rape has not been committed.
14.2.2. Incest
It means sexual intercourse by a men with a woman who is clos ely related to him
by blood (prohibited digress of relationship), example – daughter, granddaug hter, sister,
stepsister, aunt, or mother. Instances between father and daughter and brother and sister
are common. These cases usually have psychological features. Incest occur s:
– Between mental defectives who are unable to understand the prohibitions against i t,
or whose feeling are too strong to inhibit them behaving in this way,
– Where alcohol removes the natural inhibitions,
– In case of cerebral disease, such as general paralysis, seni le cerebral degeneration,
etc.
– Where a brother and sister have been separated since childhood’or for a long period
and meet later as strangers,
– Where close relations have to live in intimacy.
14.3. Unnatural offences
14.3.1. Homosexuality means persistent emotional and physical attraction to members of
the same sex. As such it is an abnormal personality development.
In this situation, the forensic pathologist may find:
– Bruises around the anus (especially discoid finger bruises),
– Hematoma is frequently seen, either as a diffuse swelling of t he anal margin, with
obliteration of the normal anal skin folds,
– Dilatation of the anus (possible also in bodies without homosexual offenc es); it is
irritable and tender to touch,
– Digital examination may show loss of especially and tone,
– Reddened margins, sometimes abraded of the anus,
– Eversion of the lower rectal mucosa through the sphincter.
– Lubricants matter, seminal fluid or veneral infection,
– Blood stains around the anus, o perineum and clothes,
– Fecal matter around the anus
In chronic passive homosexual may find:
174
– The “funnel anus” – may be also an anatomical version,
– Silvery thickening of the skin outside and at the margins of the anus – may be due
also to chronic scratching from pruritis,
– Anal prolapsed,
– But most of them have no signs.
In active agent may find:
– Sometimes the peculiar smell of anal glands transformed to the penis, and traces of
faecal matter and lubricant on the organ,
– Abrasions on the prepuce, glands penis or tearing of fraenum,
– Blood and seminal stains,
– Presence of veneral diseases.
At autopsy, the diagnosis is made – in both cases (homosexual rape a nd chronic
passive homosexual) – only form: acute damages; presence of semen or lubricants
inside the anus.
14.3.2. Sodomy
Sodomy is the anal intercourse between two males, or between a male and female.
This used to be practiced in a town called Sodom. It is also call ed “buggery”. It is called
gerontophilia when the passive agent is an adult, and paederasty , when the passive agent
is a young boy, who is known as catamite. A pedophile is an adult who repeatedly engages
in sexual activities with children. It can be heterosexual or homos exual. Any degree of
penetration or any attempts at penetration are punishable. Proof of em ission is not
necessary. When the act is performed with the consent of the pas sive agent, both are liable
for punishment, but only the active agent is punished when the offence is committed
without consent. Unless the person is drugged or very drunk, it is diff icult to be performed
against the will, for slightest resistance is sufficient to pre vent the offence. The crime is
frequent among sailors, prisoners, in hostels, military barracks for they are thrown together
for long periods. False charges may be made for blackmail, a nd men may be tricked into
homosexual relationship by men disguising as women. This type of hom osexuality is seen
among all levels of the society. When practiced between two men, they may alternately act
as active and passive agents. The sign is identically to the homosexual.
14.3.3. Buccal coitus (coitus per os or sin of Gommorrah)
According to the Bible, this sin was common in a town called Gomor rah. In this
type of sexual offence, the male organ is introduced into mouth, usually of a young child.
Rarely, faint teeth marks and abrasions may be seen on the peni s. Death may result from
175
aspiration of semen or impaction of the penis in the hypopharynx. The di agnosis is made
by finding semen in the respiratory tract or stomach. Buccal swabs should be taken or the
victim’s mouth rinsed with distilled water, which can be expectorat ed into a sterile
container, which are useful up to nine hours. It is a punishable offence.
14.3.4. Tribadism
Female homosexuality is known as tribadism or lesbianism. According to Greek
mythology, women of Isle of Lesbos practiced this perversion. Sexual gratification of a
woman is obtained by another woman by simple lip kissing, genera lized body contact,
deep kissing, manual manipulation of breasts and genitalia, genital apposition, friction of
external genital organs. In some cases enlarged clitoris is use d as organ of passion or some
artificial penis or phallus may be used. The external genitals may show scratch marks,
abrasions, or teeth marks. The practice is usually indulged in by wom an who is mental
degenerates who suffer from nymphomania. Lesbians who are morbidly je alous of one
another, when rejected may commit homicide, suicide or both.
Bestiality is the sexual intercourse by a human being with a l ower animal. The
animals involved include those that are kept on the farm or as pets in households. Because
of their convenient size, animals like calves and sheep are more o ften involved. A few of
larger birds like chicken, ducks, and geese are also involved. Other anim als used are cows,
mares, she-asses and bitches. Vaginal intercourse is the most common, but intercour se may
take place through the anus or any other orifice (example – nose). This is seen in persons
suffering from mental abnormality. Persons who go out to graze ca ttle in the fields may be
excited when alone with the animals. Sometimes, the act is comm itted due to the false
belief that gonorrhea is cured by intercourse with a she-ass. Do gs and cats are the common
animals for females. Usually the animal manipulates the genita lia with its mouth, and
actual coitus is very rare.
Signs in the accused:
– Animal faeces vaginal secretion or hair may be present on the penis. They may be
tearing of the frenum;
– Marks of injuries on the body due to kicks, teeth or claws of the animal.
– Presence of animal hairs especially of its/external genita ls on the person or the
clothes.
176
14.4. Sexual perversions
14.4.1. Sadism
Sadism- the term is derived from the name of a French nobleman, the Marquis de
Sade, infamous for his crimes and writings. Many of his stories w ere about sexuality,
cruelty, and torture. In sadism, sexual gratification is obtained or increased from acts of
physical cruelty or infliction of pain upon one’s partner. It is see n more commonly in men.
To obtain sexual gratification the sadism may bite, beat, whip, produc e cuts, etc., or ill-
treat or torture his sexual partner in many other cruel ways. It develops due to early
experiences of brutality in relation to sex.
14.4.2. Masochism
This term is derived from the name of Leopold von Sacher-masoch, an Aust rian
novelist. Being whipped by his wife used to be a stimulant for his literary work. This
condition is the opposite of sadism. In masochism, sexual gratificat ion is obtained or
increased by the suffering of pain. Masochists get pleasure from being beaten, abused,
tortured, humiliated, enslaved, degraded or dominated by their sexual par tner, and they
tend to place themselves repeatedly in self-defeating situations. Such painful stimuli may
entirely replace the ordinary sex stimuli. It is usually found in males but i s may be found in
females, who may willingly expose themselves to the risks of se vere bodily injury or
murder at the hands of brutal husbands or lovers.
Sadism and masochism are rarely found in a pure state. They are usually found as a
combination with one type dominant over the other. The combining of these pra ctices is
called bondage . They are found in all age groups and in all socio-economic levels. The
acts of cruelty or pain associated with sado-masochism may s evere as a stimulant for, or as
a complete substitute for sexual intercourse.
14.4.3. Necrophilia (philia = to defile or foul)
In this condition, there is a desire for sexual intercourse with dea d bodies. It is said
to have sado-masochism foundation and that decomposition, foul smell, and coldness act
as stimulants. There is also no danger of rejection or resistance . The offence is usually
committed on a newly buried corpse or a body awaiting burial. T he corpse may be
mutilated following intercourse. Murder for the purpose of necrophilia is very rar e.
14.4.4. Fetichism
A fetish is an abnormal stimulus or object of sexual desire. Feti chism means the
use of such objects for sexual gratification. In this, the person exp eriences sexual
excitement leading to orgasm from part of the body of a woman or some article belonging
177
to her that normally has no sexual influence on the mind (example – unde rclothing,
brassiere, petticoat, stocking, shoes, etc) which act as substitut e for the female love object.
The fetish may be only incidentally associated with human body (exa mple – flowers). In
some cases, a picture of the fetish object provides sufficient st imulus. Sometimes, the act
of stealing the articles provides adequate sexual satisfaction, t hough often the fetish article
is stored to the satisfaction of the fetish, or touching it gives him sex pleasure, or he may
masturbate into the object. It is almost exclusively seen in mal es. It is harmless, but rarely
it may drive the person to obtain his fetish objet through violence, or other criminal act
(example – objects may be stolen, or women may be attacked either as part of robber y with
violence)
14.4.5. Masturbation
Is the deliberate self-stimulation which effects sexual arousa l. Mild masturbation
exercises are common both to men and women and are of little importance. Techniqu es are
largely manual, by moving the penis against a bed or other object. Ur ethral insertions and
anal stimulation and anal insertions are rare. Hollow articles l ike bottles, test tubes, etc.,
are sometimes used, or articles made of rubber and plastic which s imulate the female
genitalia are used.
The female, a finger is gently and rhythmically moved over clitor is or labia minora
or steady pressure is applied over these parts with several fi ngers or whole hand. The
genitalia may be rubbed against a pillow, a bed or some other object , sometimes, women
may insert fingers, wooden rods, glass tubes, metallic bars, banan as, etc., or artificial
masculine genital parts made of rubber or plastic into the vagina. Masturbation is an
offence only when practiced openly (example – telephone booths, lavatories)
14.4.6. Exhibitionism
It is a willful and intentional exposure of the genitalia in a publ ic place while in the
presence of others, to obtain sexual pleasure. It may or may not be accompanied by
masturbatory acts. It is done mostly by males, often to children or the persons of the
opposite sex. The pervert adopts a childish method of attracting attent ion to himself, to
experience sexual gratification at the time of the exhibition, wi thout physical contact. In
some cases, the act is premeditated. Occasionally, women may e xpose themselves in
public. Majority of them are psychopathic or suffer from compulsion neurosis.
14.4.7. Frotteurism
Is contact with another person in order to obtain sexual satisfacti on. Sexual
satisfaction is obtained by rubbing against persons in crowds. If they attempt intercourse
178
they have a premature ejaculation of they are impotent. It is an uncommon perversion and
rarely occurs alone.
14.4.8. Undinism
In this the sexual pleasure is often obtained by witnessing the ac t of urination by
some one of the same or opposite sex. In some cases pleasure is obtained by be ing urinated
upon by the loved one or in urinating on him or her, but this is a rarity.
14.4.9. Voyeurism
It is the counterpart of exhibitionism. The voyeur must see people undr ess in order
to be sexually satisfied. The perversion is in the sexual dependence upon “looking”,
“peeping”, “seeing”. There is a morbid desire to look at the sex ual organs or other usually
clothed parts of the body of one of the opposite sex, at to watch sexua l intercourse as a
source of sexual satisfaction. The act of observation can also resul t in attempts at
exhibitionism or masturbation. This perversion occurs in case of se ver sociopathic
personality disorder. To many males, observation of a female who i s undressing may be
erotically more stimulating than observing her when she is fully nude . Usually such
persons do not commit a major sex crime, but sometimes they may assault the victim, or
commit a murder. It is rare in females.
14.4.10. Transvestism
A transvestite is a person whose whole personality is dominated by the desire to be
identified with the opposite sex. The term is derived from the name of Chevelier d’Eon
Beamont, a Frenchman, who preached this. He wants to be thought of as a member of the
opposite sex. His dress, manner, occupational interests and associati ons are all designed to
increase his feeling of being a woman. Sexuality with him is relatively unimportant except
as it promotes his feelings of feminity. There are varying deg rees of transvestism. It is
usually found in the males who obtain sexual pleasure by wearing f emale dress.
Psychologically, it may depend upon an individual’s erotic attraction f or opposite sex.
Sometimes it depends upon an individual’s violent attraction against his or her own sex. It
such a case, he may or may not be erotically attracted to oppos ite sex. Only small
percentages are homosexuals. Rarely, it develops out of a fetishis tic interest in clothing or
some part of opposite sex. Many cases are associated with sadom asochism. There is no
hormonal disturbance or genital abnormality.
14.4.11. Sexual Oralism
It is the obtaining of sexual pleasure from application of the mouth t o the sexual
organs. It is a common perversion, both heterosexual and homosexual. Fellatio is the oral
179
stimulation or manipulation of the penis, either by the female or ma le. Cunnilingus is the
oral stimulation of the female genitalia.
180
CHAPTER 15: DNA GENETIC FINGERPRINT
AND IT S IMPORTANCE IN MEDICO-LEGAL PRACTICE
15.1. Theoretical appreciations
15.1.1. Getting started on the molecular biology of DNA
For the moment, modern genetics can be fixed in 1900, with the rediscover y of
Mendel's rules. The word "gene" was printed for the first time i n 1909. The first genetic
map showing relative location of genes on chromosome 6 was published in 1913. L ater
research made in the human project, consisting of DNA identifica tion code of an organism
living cells have shown that this code is the support of heredity, i. e., absolutely unique
fingerprint, a genetic, of each individual.
From a structural point of view DNA is a polymer, a large molec ule is formed by
linking together a series of units (nucleotides) that are repea ted, the number of about 3
billion. Nucleotides are divided into four types, designated by the letters ACGT
conventional – A =adenine C = cytosine, G = guanine T = thymine and grouped along a
twisted tape, whose structure was named "double propeller "or double he lix. Specific
sequence of these four types of bases determines all the att ributes of a person's genetic.
Properties of DNA molecules are directly determined by its physical str ucture.
In the double propeller, each containing a nucleotide base is wrapped ar ound each
other, which is composed of two chains or nucleotide monocatene. Each nucle otide in a
chain link of a chain of parallel nucleotide is thus sufficient f orces for the two monocatene
be maintained. Pairing of the bases of two nucleotides on the two paral lel chains is
extremely specific, meaning that an A nucleotide with a nucleoti de mate only with T and
G respectively with C. This pairing only mandatory, called complem entary base pairing is
exploited in all systems of DNA typing. When the double helix is inta ct it is said that DNA
is double stranded, and when the two strands apart in kind or in test tube , called single-
stranded.
In nature, the complementary base pairing is responsible for the abi lity of DNA
molecules to replicate (copied exactly), which ensures transmi ssion of genetic information
across generations. During replication double helix is opened in the t wo strands of specific
enzymes and new units (nucleotides) are attached one by one on both the principle
monocatene specific pairing (AT or TA and GC or GC respectively) . Thus, using a chain
as a matrix, summarizes the other chain is perfectly complem entary to the first, resulting in
181
two double-stranded DNA molecules identical to the original. The orde r of bases on the
new chain is determined by the old chain. This product can be replic ated today, the tube
and forms the basis of polymerase chain reaction (polymerase chain reactio n "-PCR).
Short segments, complementary single-stranded DNA, present in vitr o a specific
affinity for each other, their pairing is done on the same principle s of complementarily of
the bases. In appropriate circumstances, fragments of DNA are c omplementary each other
and joined, forming double molecules. From a technical standpoint, this proce ss is called
hybridization.
15.1.2. Variability of the genome sequences of bases
In scientific investigations, especially through the study of vari ous diseases have
been detected in different places in the DNA base sequence vari es greatly from one
individual to another. A molecular location (the DNA) is called locus . The existence of a
population of more than one allele of a marker for the same locus is called polymorphism
(an individual can have at least two alleles FOR A same locus, namely locus because it
possesses two copies). If such polymorphic loci have an extremely large number of
variants (hundreds) is said locus is hyper-variable. Variations or pol ymorphisms are
caused by the sequence of bases in a particular locus or DNA fragment leng th between two
points defined. Sequence polymorphisms are similar. Length polymorphism may well be
likened to a train that has a different number each time cars. Loc omotive and wagon-mail
(last car) delimit the ends of the train, and the total length va ries depending on the number
of cars attached between the ends. Each car is the same DNA s equence. In genetic
terminology, the coaches are called tandem repeats. A locus showin g variation in number
of tandem repeats locus is called with variable number of tandem repetitions (VN TR).
15.1.3. The role of enzymes in molecular genetics processes
It is impossible to discuss the biochemical reactions, without refe rring to the
enzymes. The enzyme catalyzes the addition of nucleotides in a DN A molecule is called
polymerase. Restriction enzymes are another class of enzymes t hat are able to break DNA
molecules into shorter fragments. In nature they exist in bacter ia to protect them from viral
infections. Restriction enzymes recognize short sequences, specific vira l DNA at this level,
it is broken into fragments. Bacterial DNA cannot be attacked b y these enzymes due to a
protective mechanism. Special molecular biology enzymes were is olated and used them to
break the DNA molecules of any type in the sequence that the enzym e recognizes. Each
enzyme can only break a DNA molecule in the sequence that it recognizes.
182
15.2. DNA Profile – scientific and technological advances.
DNA profile based on the fact that DNA carries the portion o f its non coded (non-
carrier genes) repetitive regions (between 200 and 14,000 repetitions) called VNTR
(variable number of tandem repeats) of some identical sequences c omposed of four bases
delayed (adenine, thymine, cytosine and guanine). These sequences ar e constant and
specific to each individual and are transmitted as groups of blood unde r the laws of
heredity in the DNA of each parent. Only univiteline twins have the s ame sequence. Two
unrelated people have the opportunity to present a sequence identical to a trillion. The
brother’s chance is 1 in ten billion.
Establishing a DNA profile is a process that starts from the moment a tiny amount
(0.20 ng) of DNA genetic material is taken from the scene and ends when the sample is
assigned to a computerized numerical value as a "great code. Compar ing the DNA profile
of a person with a sample of DNA found at crime may help eliminat e some suspects and
guilt forever may be the clue.
There are several methods of obtaining DNA profiles. Method was used initially
scanned, a method that is based on the principle of the sample DNA cleavage by restr iction
enzymes, electrophoresis for viewing these fragments and compari ng profiles obtained
from the circle of persons suspected or database . This method is l aborious, but that the
genetic material to be analyzed integrity and relatively hi gh quantity and time is
considerable.
Because of the method put in place "polymerized chain reaction (PCR ) the amount
necessary to complete a DNA analysis has diminished considerabl y. This new technique
allows the multiplication of DNA millions of times the quantity of a sample with greater
speed and accuracy.
Amplification process allows both the investigation of biological mat erial was
degraded and traces amounts of intact material containing enough DNA for an anal ysis.
Consistency between the observed DNA sequence of a suspect and a sampl e turns
out perfect, and the probability of a fortuitous match the sequences of two individuals are
extremely poor.
A newer method called "Short Tandem repeats" or STR (short re petitive sequences) is
based on the observation that certain DNA sequences vary considerably from individual to
individual. Comparing several STR sequences, it becomes possible to obtai n an exclusion
probability of correspondence or higher.
183
15.3. Advantages and disadvantages genetic fingerprinting method
Specifically this analysis has the following advantages:
Identify characteristics of individuals and not by large groups such a s the four
blood groups or the 6 groups suitable for serum samples collected from t he crime
scene.
Do not lose the characteristics of individual "personality" in the m ixtures (mixtures
of blood or secretions) being able to detect the contribution of the perpe trator or
the victim.
Very small sample is necessary in some cases, even if the sample is distortion
caused by environmental factors, can be analyzed, in which result the classical
methods fail.
The possibility of automation – are a great advantage, being removed human error
and bias interpretations of results.
Possible analysis in computer memory storage – result in data b anks that can be
used by overlapping genetic fingerprints of offenders discover l ater (the principle
is the same as that used in the AFIS system).
Removal of the case, the suspects quickly and completely innocent.
Early identification of perpetrators based on a presumption paternity.
Increased public confidence in the justice system and crime reduction.
All these advantages with specialist expertise and regulation of the judiciary, have led EU
countries to be used exclusively genetic fingerprint expert, is aba ndoning the other
methods. It should be noted that there are some disadvantages:
Performance grade (probability of identifying the person) depends on the technique
used (usually using several methods) and the level of specializ ed and experience
technicians.
Admissibility of evidence could be appealed, invoking the so-called "brot her
defense", the family person guilty – in which case the victim DN A profile could be
part of the same bands because they have a common ancestor. Ignoring this issue
would mean violating the constitutional principle of presumption of guilt.
Quality of analysis, the equipment used, specific reagents and techni cians readiness
determinations lead to higher costs. Drastic aseptic conditions re quire extreme
precautions taken in handling biological samples. Simultaneous use of ge netic
methods, nucleic acid fragments and reagents multiplication, possibly i nter-
contamination evidence or their contamination by staff, where securit y measures
184
are not met (fence aseptically sterilizing grade of the room , reagents, utensils and
accessories).
Investigators and prosecutors have used DNA profiles should be aware tha t defense
attorneys will discuss if certain issues, the admissibility of this evidence. All major points
at issue are the following:
Possible contaminations of samples, which can lead to erroneous results interpreted
or even their complete invalidation.
Comparison with a population insufficient to calculate probabilities.
Handling of specimens in poor condition or lack of reliability of labor atory
procedures.
15.4. Scope of genetic methods
Genetic methods find applicability for the whole range of crimes, namely:
For murder, genetic profile will be determined based on traces of blood (dried or
not) that will compare the fingerprint of the suspect and the victim obtained based
on blood samples from him.
For rape, genetic profile determination analyzing sperm recovered f rom the
victim's vagina will be compared with the suspect's DNA profile obtained on
removal of a sample of blood from it. In the case of rape, sexual pe rversion or
crime of pedophilia can individualize each participant mixtures of fluids.
In case of traffic accidents, products on the road, fleeing the sc ene of the accident,
whether human material found on the vehicle body, the genetic profile wi ll be
established based on cells taken from the machine and compared with t hat of the
victim. If the correlation is clear that the vehicle carrying the biological trace that
injured victim.
Theft and related offenses by the traffic safety on public roa ds are the most
common and most susceptible to leave traces of which will be subsequent ly taken
DNA samples.
Gentle methods are used in the study of same fatherhood (see for ensic examination of
parenthood), in this situation is necessary to analyze three sets of DNA (from mother to
child and the alleged father).
Also, these methods are used to identify corpses (those with unknown ide ntity,
skeletal, victims of catastrophes, terrorist attacks, aviation a ccidents, fires). To identify
the corpses, one solution would be to determine parentage in circumstances which are
185
presumed ancestors or descendants. In this situation, the key role is held by
mitochondrial DNA is much harder to destroy.
Genetic methods are also used in:
Identify the species to distinguish the different human or animal origin of
biological products;
Identification of different blood samples taken for analysis;
Where required reopening of cases pending or verification of possible m iscarriages
of justice;
The formation of genetic fingerprints of criminals banks but also of some
populations.
15.5. Value and limits of DNA profiling as evidence in court
The controversy over the probative value of genetic fingerprinting appeared
expertise, as we showed with the first uses of genetic finge rprints in forensics and
criminology. Forensic experts adapt the technical, scientific i dentification of legal issues.
Besides the fact that some tracks are taken from the scene in small quantities, they
sometimes contain unidentified contaminants that can sometimes le ads to errors when
conducting surveys. The position of the court to these incidents illustrat es the difficulties
in assessing the method.
From the outset of justice to the world several scientific quest ions, whose answer is
fundamental to the use of DNA analysis as evidence in forensic inves tigation. On these
questions, researchers involved in the human genome project have come up wi th answers
clarifying every aspect of them.
First, the sample size has been demonstrated scientifically a nalyzed to determine
the DNA can be reduced to the size of molecules, DNA is present in a living organism and
every cell (except erythrocytes), regardless of what part of the body come .
The age of biological samples, the dilemma was resolved by rese arch carried out
on samples whose length exceeds several thousand years (Egypt mummies).
In terms of strict demarcation between the DNA of living org anisms, species and
subspecies, research the past 25 years have solved the problem. The use of human markers
and there is no possibility of hybridization probes human fragments wit h fragments from
other species that might be contaminated sample legal interest.
The fact that DNA tests may be done by very small amounts of samples from live
bodies at home, that their age is not considered an impediment to the ir determination and
186
composition of the complete human genome map, which excludes the possible c onfusion
of DNA human with non-human DNA, less known, give a DNA analysis chara cter single
test samples. In these circumstances, the findings about the exist ence of DNA, is
equivalent to decrypt the key to any code.
Discussions on the reliability of genetic fingerprinting tests , stresses the importance
of evaluation rigor of scientific methods of legal identification. F or this reason, surveys are
conducted based on techniques developed by EDNAP (European DNA profiting Gr oup –
European Working Group for DNA). The European group formed in 1989 is composed of
scientists belonging to laboratories in Europe using genetic fing erprinting method's
practical and have proposed to work on the standardization of internationa l cooperation
work. The results of the first series of experiments were publis hed in 1991 proving that
standardization is possible when working laboratories follow the same protocols. This
standard protocol common to all practitioners will allow genetic f ingerprints obtained in
different countries, and existing research to determine causes of error s.
Aware of the stakes of this expertise, scientists from the for ensic laboratories
submit their analysis of common self-controls. In addition an independent control system,
national and even international levels is essential.
15.6. Collection and preservation of biological samples for DNA determination
Ability to perform DNA analysis of successive biological evi dence from the scene
depends very much on the type of material and the way it was prese rved. Thus, the
technique used to harvest such evidence, the quantity and type of biological material to be
collected, how the biological material must be packaged and how its cons ervation program
is the sensitivities of forensic DNA testing. On the one hand, i f it is not properly supplied,
its origin can be questioned, since being moved improperly, can occur s econdary
contamination. If the biological material with DNA is not properly preserved, it may
deteriorate. All these effects will seriously affect the DNA analys is.
Early stages examination done help physical evidence at both crime scene and
forensic laboratories. Forensic documentation is important from two points of view:
scientific and legal. You do not have damaged anything until the init ial position was not
recorded. Every major piece of evidence should be recorded.
Evidence at the scene:
• Photos and video evidence before being touched, moved or harvested.
187
• Observing location and conditions under which evidence is.
• Observe and sketch the distances between the evidence and other objects at the
scene.
• Observe and sketch the conditions of biological evidence.
Evidence from forensic laboratory:
• Observation of packing and sealing, labeling samples.
• Initial package with unique identification marks, case number and date.
• Check no. and comparison with permissible form to ensure that the corre ct item
was received.
• Observe, sketch and photograph received item.
• Check if the article meets the conditions of admission and if his de scription is
correct.
• Photography, designing and evaluating biological evidence before sampli ng
location.
• If the preliminary test was carried out, there will be and how t est results. Always
wear gloves and to prevent contamination.
15.7. Harvesting, transportation and storage of evidence
When biological evidence has been transferred directly or secondari ly, this area
will remain bound by absorption or adherence. In general, biological mate rials will be
absorbed liquid and solid join. The method of collection depends on the condition in which
the biological material.
15.7.1. Blood and blood stains
Liquid blood samples.
Blood from a person.
A. Blood fluid from a person
a). Liquid blood should be collected from a person qualified medical personnel.
b). It is collected in two tubes of 5 ml each using EDTA as an anticoagulant.
c). each tube should be labeled with date, time, name, name of harvestin g, no. of cases and
exposure.
d). Blood samples are placed in the refrigerator (not frozen) and sha ll be given in as soon
as possible.
188
B. liquid blood at the scene:
a) Blood is collected liquid with a clean syringe (sterile) or with a pipette and transferred
into a clean tube (preferably sterile).
b). A blood clot can be transferred to a clean tube with a clean spatula.
c). A piece of clean cotton may be used to absorb liquid blood or blood clot.
d). Samples will be labeled as no. case no. Article, date, time and name of the harvest.
e). If dried blood samples are collected, they must be preserved in an anticoagulant,
refrigerated and brought to the laboratory as soon as possible.
C. Blood samples fluid from snow or water:
a). Samples found blood on the snow or water must be taken to prevent dilution.
b). It removes a large quantity of these samples as in a recipi ent clean to prevent
contamination.
c). Samples are labeled as described above.
d). It freezes.
e). Bring to the laboratory as soon as possible.
D. wet blood stains
Wet clothing with blood stains:
a). Clothing that is wet bloodstains should be put on a clean surface and allowed to dry.
b). It will not never have put in a plastic bag or a sealed recipient.
c). Doing so may lead to contamination and bacterial growth and thus damage the sam ple.
d). After the clothes and the stains are dry, be packed in a conta iner of paper that will be
labeled correctly.
E. Objects wet blood:
a). Small objects to be dried blood stains wet and then harvested.
b). There must be blood stains integrity during packing and transportation.
c). At the scene there can be big things wet with blood stains. The y should be transferred
to a clean piece of cotton.
d). That piece of cotton should not be allowed to be used before being wrappe d in a paper
container.
e). Each of the objects and the container must be labeled correctly.
F. Dried blood stains:
Dried blood spots on transportable items.
a). Dried blood spots on arms, clothing and other portable objects must be collected
separately.
189
b). Each item is individually placed in a paper recipient be sealed and labeled.
Dried blood spots on solid surfaces absorbing objects.
a). The blood spots should be documented and the requirements outlined in question.
b). The stain can be harvested by scraping on a clean piece of paper.
c). That piece of paper must be placed in a sealed envelope.
d). Each sample must be labeled correctly.
Dried blood spots on large objects or non-transportable, where spots cannot
be scraped and the objects that cannot be cut.
a). The blood spots should be documented that outline requirements.
b). Blood stain can be dissolved in sterilized saline solution by rubbin g the stained piece of
cotton.
c). The piece is left to dry and then put in a package of paper.
d). Then the package is placed in a sealed envelope and labeled.
e). This process can be controlled by taking a spot from an adjacent area, but spotles s.
Blood stains on carpets, upholstery and other items that cannot be cut.
a). Stained areas should be prepared as described above.
b). A portion of the object they are blood stains can be removed with a sharp instrument,
clean.
c). Each piece should be cut separately packaged and labeled.
d). To be harvested and a portion control without bloodstains.
Small drops of blood dried:
a). It is often difficult to harvest the drops of blood. It is possible that they are harvested
using adhesive tape.
b). After appropriate preparation, the method can be used duct tape to drops of blood on
some surfaces.
c). Each piece must be wrapped and labeled.
d). Then put it in a plastic container.
e). Suspend the strip with blood drops in the middle of the container.
f). Shall be sealed and labeled container.
15.7.2. Sperm and semen stains.
Semen samples found at the scene.
a). Evidence of sperm being cataloged by observing, recording, video and drawings.
b). Use a clean syringe to transfer semen into a sterile tube.
c). No labeled tube, case, the date, time, location and name of the harvest.
190
d). The sample is kept in the refrigerator and bring to the laboratory as soon as possibl e.
e). Alternatively, the semen can be transferred to a clean piece of cotton by acquisition.
The piece of cotton is then dried, packaged, sealed and labeled.
Semen stains on portable objects
a). Semen stains on clothing, bedding, pillows and other portable objects to be collected as
such.
b). If an object is wet spots on it, they should be left to dry before being harvested.
c). Each item must be packed separately in a container of clean paper.
d). Each item must be sealed and labeled.
e). Objects must be kept refrigerated and sent to the laboratory as soon as possi ble.
Semen stains on the big things that can be cut:
a). These objects are: carpets, bed linens and upholstery.
b). It catalogs the sample as described above.
c). Use a clean knife or blade to cut the spots.
d). The sample packs to secure and prevent any contamination.
e). This package is placed in a container, sealed and labeled.
Semen stains on absorbent surfaces and non-transportable:
a). They are: floors, counters and metal surfaces.
b). It catalogs semen stains as I described.
c). It uses a scalpel to scrape clean the semen stains on a cl ean paper and place in a
container.
d). Clean the knife before each use to avoid contamination.
e). Each container must be sealed and labeled.
15.7. 3.Tissues, organs and bones.
Tissues, organs and fresh bone.
a). Each sample should be described and documented by sketching, photogr aphy and
filming.
b). This type of evidence can be collected with a clean forceps.
c). Each item should be placed in a clean container without adding fixers.
d). Each container must be sealed, labeled and stored in a freezer.
e). Samples should be brought to the laboratory as soon as possible.
Tissues, organs and old bones.
a). Front on each sample to be harvested must be photographed and sket ched. Note the
size, shape and distances between samples.
191
b). Each sample should be collected with clean gloves.
c). We must be careful not to contaminate a sample to another, and the refore change
gloves for each sample.
d). Each sample must be placed in a clean container that is sealed and labeled.
e). Samples can be stored at room temperature and taken to the labo ratory as soon as
possible.
15.7.4. Urine, saliva and other body fluids.
Liquid samples.
a). Liquid urine or saliva must be transferred into a clean container as soon as possi ble.
b). The container should be sealed and labeled.
c). Samples must be refrigerated and brought to the laboratory as soon as possible .
Stains
a). Stains, saliva and urine can be collected as such or by scraping.
b). Each sample is placed in a container of clean paper.
Harvested by scraping spots put them in a clean paper envelope that is placed in a
container of paper.
c). Samples must be sealed and labeled.
d). Samples must be taken to the laboratory as soon as possible.
Hair samples.
a). Hair samples must harvested with clean tweezers.
b). Each hair sample must be packaged separately and then sealed and labeled.
c). Harvesting should be done carefully to avoid damage to the hair root.
d). Hair mixed with blood, tissues or other body fluids should be treate d carefully. Each
sample must be placed in a clean container, then sealed and labeled.
e). Samples are stored in the fridge and go to the laboratory as soon as possible.
15.8. Peculiarities of identifying, harvesting, packaging and preser ving biological
traces or micro-traces present at the scene for crimes of murder and their
possibilities for recovery by the method of genetic analysis.
Genetic profiles can be obtained from any trace of biological or m icro-traces
containing several nucleated cells. These objects can be identifie d by clothing, skin, or
different surfaces of objects. Statements by the victim can provi de information about
places where biological traces from the author – for example if the victim scratched the
skin of the author or to have used various tools and objects touched surfaces.
192
Any part of the victim's body where the author had a contact in t he form of kissing,
sucking, licking, biting with this, there are epithelial cells, harve sted and analyzed
properly, can lead to identifying the offender.
These traces of biological or micro-traces may be harvested from:
15.8.1. Victim
Body surface of a murder victim may submit a series of marks or copyright micro-
traces from secretions or as a result of interaction with the body parts of the author.
In areas of bruising on the body there may be some biological m icro-traces which
can be valued in terms of genetic analysis.
At a microscopic examination of body surface area bruises caus ed by pressure,
friction or impact by the author, we observed numerous cells in the e pithelial layer off, and
some of them may come from the author.
For sampling, it is required following materials: gloves (sur gical), sterile swabs,
sterile water or saline, or other objects blunt scissors, paper pa ckaging and protective
mask.
Sampling is done as follows:
– Take a sterile swab and moisten with sterile water.
– Shift slightly over the end of his cotton zones, so you can harvest the majority of
epithelial cells to the author, present the victim's skin. A sharp f riction pad will cause the
victim's skin epithelial cells from the majority of it is in quantity, which is not desirable.
– Remove unused end with a sterile scissors.
– Buffer under absolutely sterile dry place away from heat or s unlight, or if not possible be
kept at 4 degrees C until reaching the laboratory.
– Properly packaged and labeled the two envelopes with the name of the person from
whom it was collected, date and area where it was collected.
These micro-traces can be found in the following modes of action of the aggr essor:
– Freehand bottleneck where bruises were formed;
– Catching, collecting and dropping off the victim's hands by the author;
– Hitting with fist, palm or other body parts poster, which also forms bruising.
In the case of identifying the biological traces are visible, the y can easily be taken
by scraping, and if they are wet can be transferred to sterile gauze pads, by dabbing the
area concerned, then be properly dried, then packaged in envelopes that ensure their safety
and kept at 4 degrees C.
193
Hairs found on the body are harvested as described above. There are s ituations in
which they can be seen individually or, sometimes, are among the victi ms. In this case we
use various techniques for taking all or a significant number of thr eads, and in the
laboratory, based on morphological examination, to be selected those showing differences
or similarities. The genetic material if the hair is found in the epithelial she ath (bulb).
If the victim was immobilized using objects such as: ropes, belts, handcuffs, etc. or
was strangled, they can contain sufficient traces of biologica l or micro-traces coming from
the author, links to training in areas that can be identified by genetic methods.
Because these objects have dimensions that allow transport in the l aboratory is appropriate
to comply with the harvesting and conservation outlined above.
15.8.2. Victim's clothing items.
Victim's clothing items can often demonstrate that they were forced, if fractures or
other signs, such as soil. If they cannot be identified other type s of marks (blood, semen,
saliva, etc.) may contain micro-traces biological fracture zone s from the person who
created them as epithelial cells.
Most of the victims' clothing or objects bearing a set of traces and biologica l micro-
traces which capitalized by genetic analysis can provide useful evidence in solving cases.
Clothing items may be carriers of the victims of the followi ng types of signs or biological
micro-traces blood, secretions (saliva, semen, etc.), including dandruf f, vomit, feces, hair,
tissue fragments. It indicated that the samples sent for analys is to be subject to the
conditions of collection and preservation of evidence.
15.8.3. Traces and biological micro-traces in vicinity site of the victim.
In this area can be found traces or micro-traces individual or mix ed, deposited on
various supports, such as those listed above, or objects, tools, weapons were used by the
author in the crime: gloves, pieces of gloves, condoms, masks or other obj ects not
belonging to the victim's clothing, remnants of cigarettes, etc.
Items bearing such marks are very numerous, it is important that they be identified
and clearance, preservation, packaging and sending for review must meet the requirements
specified above.
15.8.4. Traces and biological micro-traces inside or adjacent to the offense cond uct.
Copyright Micro-traces from the scene of the crime may be pre sent in various
places and objects "key" such as door handles, electrical switches, windows, weapons that
have been accessed "mandatory" for committing criminal act.
194
Other objects or surfaces in the production of the offense may be ca lled auxiliary –
glasses, cups, bottles, cutlery, etc. and they can keep the tracks from the author .
For all these cases are shown that objects bear to be sent to the laboratory after
being photographed at identification. If this is not possible micro-tr aces will be harvested
from such areas. Traces of blood can highlight and alight. This method is used only to
determine traces of blood that is not seen with the naked eye.
It is indicated for use as the first method to identify and micr o-traces traces of
blood, it must remain the last method.
15.8.5. Transfer micro-traces traces from the victim or the item s of clothing or other
things of the author.
In the same manner that leaves its own traces author or biological micro-traces
crime scene and the victim can transfer them to his body, clothi ng or other objects of the
author.
One of the samples taken from suspects which is the repository under the nails.
Nature Nail physiological disposition allows a certain amount of m aterial storage
underneath, depending on size. If contact with your free hand form of com bat, and the
author of a murder victim or body fluids from achieving this, the nail may accumulate
greater or lesser amounts of biological material.
The collection traces the store or micro-traces under the nails should be made only
from the superficial layer of deposit under the nails, which is t hen packaged and canned.
This procedure is repeated for all deposits under the nails. If possibl e, it is shown that such
nails to be cut without disturbing the deposit and thus sent to the labora tory. Harvesting
and packing is done separately for each finger.
15.8.6. Crime weapon.
In any hard object may be hiding a murder weapon, but the information t hat can
accumulate over IP will reduce the search to a few types. On the surface of any firearm, it
can be taken micro-traces of biological genetic profiles that c an get the owner and / or the
person who used it.
These are existing biological micro-traces superficial laye rs, as a result of contact
with the person uses as well as in deeper layers as a result of contact with the person who
maintains it. Ideally, biological micro-traces collected ext erior or interior surfaces to be
realized laboratory microscope to identify them and avoid contamination, or they are
properly packed and sent for analysis. If this is not possible biologi cal micro-traces
intuitive collection is made of the techniques described above.
195
In all cases indicated that the weapon itself is sent to t he laboratory, packaged and
preserved properly, without trying to trace or micro-traces sampling.
15.9. Types of biological samples necessary for recognition of corpse s with unknown
identity based on genetic molecule
Genotyping in these cases is carried out:
Reference biological samples taken from dead bodies, pieces of ti ssue (muscle,
bone, skin, hair bulb harvested) or blood.
Biological samples determine membership (one of the options below).
• References collected from parents (at least the mother).
• References harvested at least one natural child.
• micro-traces deposited biological objects suspected of dying of the particular toothbrush,
razor, comb, clothes, articles that have been used exclusively by the person suspected to be
missing, etc..
Identification is made based on tests of ancestry, parentage or identity of the
genetic profiles of DNA extracted from these biological samples.
196
CHAPTER 16: GENETICS AND SEROLOGICAL LEGAL MEDICINE
16.1. Forensic genetics. DNA profile.
As I mentioned in the previous chapter one of the areas of application of genetic
fingerprinting, DNA profiling that is parenthood expertise (see Chapt er DNA genetic
fingerprint).
The parentage of the child sequence identical genetic sequence come s from the
same genetic mother and biological father by Mendelian transm ission. Compare the results
of electrophoresis of the sequence of the sequence the child mother. Those electrophoresis
fractions of the child sequence are not found in his mother's sequence, it must be fully
reflected in the sequence if it is truly the father biological father. Exclusion probability is
99.99%.
16.2. Expertise parentage. Forensic serology.
Reasons for applying for affiliation expertise:
Civil cases: establishing parentage to the mother, the father (paternity) .
Criminal cases: incest, rape.
A forensic examination of evidence of parentage through several stag es which in order
are:
Serological;
Dactiloscopy;
Anthropological;
DNA profile.
16.2.1. Expertise parentage.
16.2.1.1. The father Parentage
Is required when there are inconsistencies between legal and biological father .
Denial of paternity (for children born within marriage) with in 6 months of
finding out the news
Action brought by the father against the child.
It is based on the following legal presumption of paternity:
• The child born during marriage is the legitimate father of the m other's
husband, and
197
• The child born less than 300 days after the dissolution, annulment or
declaration of nullity of marriage, the father is her former husba nd, if he
was conceived during the marriage and whether this time the m other has
contracted a new marriage.
Establish paternity child born outside marriage: within one year after childbirth.
Action brought on behalf of the child's mother against father.
A man may be excluded from paternity in two cases:
• Identification of a protein to the child who is missing from both the mother
and the father in question (e.g. child, parents O).
• Establish that the child missing genes would have to be present in
transmission from the father in question. Possibilities:
o when the father is homozygous for a gene that is not the child (e.g .,
HR system and the child's father CC cc).
o Heterozygous for genes that is not present in children (male AB, a
child).
Exclusions based on 1 and the second is called the first order (direc t), while those
on the second second-order (indirect) and this is because the homozygous state is not
unambiguously detected but a presumption.
Usually the man is not excluded from paternity and fatherhood is confirmed.
Axiomatic that a woman is alone on an island with ten men, of which 9 are excluded, the
tenth will be declared the father of the child to be born even if he is confirmed.
16.2.2. Parentage from mother
It is required when the child has no birth certificate (unrecognize d / undeclared /
unregistered by the mother) when he was lost or abandoned or changed / stolen. Action
introduces the child on his behalf against the mother.
16.2.2. Forensic serology
16.2.2.1. The laws of heredity transmission:
Laws Bernstein:
• An antigen may occur in the child only if one parent is present.
• Whether an individual is homozygous for an antigen (eg AA), it must appe ar to
all his descendants.
198
Laws Lang:
• The progeny of the first generation occurs only if the Dominos (uni formity of
the first generation hybrids);
• The second generation characters appear and parental recessive ge nes have
been blurred by the effects of dominant in the first generation.
Laws Mendel:
• Gamete purity law (the law of segregation characters) refers to a couple of
genes, only two contrasting features of the same character (t raits allelomorph).
Alleles of a couple of genes from parents to the progeny do not mix. The
parents themselves are in relationships alleles, but it segreg ates progeny. In this
way it is possible that recessive alleles occur in the prog eny and thus double
dose to manifest phenotypic ally.
This statement allows the following basic principles:
MM + MM = MM 100%
MM + NN = MN 100%
MM + MN = MM 50% + MN 50%
MN + MN = MM 25% + MN 50% + NN 25%
• Law association (independent segregation of characters) refers to several pairs
of genes. Under this law, the transmission to the progeny of alle lomorph
features belonging to two or more characters, each character t akes place, one
from each parent. Heritage features are based on chance (for exam ple, can
inherit only recessive alleles or only dominant alleles, or only one dominant
allele and one recessive allele).
16.2.2.2. Serological classification systems used in parentage
Erythrocyte antigenic systems
Major blood groups: ABOH, Rh, MNSs.
Minor blood groups:-Cellano Kidd, Lutheran, Duffy, Lewis, etc.
Erythrocyte enzyme systems: creatine, phosfogluco-Move, esteras e D, erythrocyte acid
phosphates, glucose 6-phosphate dehydrogenase, adenylate kinase, glutamat e
transaminase priuvat, adenozindeaminaza, 6-phospho gluconate dehigrogenaza,
pseudocolin-esterase, etc.
Systems of serum proteins: haptoglobinele ( α2 globulin with three phenotypic forms II,
2-I, 2-2), group specific component, hemoglobin, etc.
199
HLA System.
Other systems: SECRET / SMT, taste / merchant.
DNA.
Phenotypic expression of a gene is called a genetic marker. It i s expressed in the
form of quality immunological and morphological characteristics. Bioc hemical and
immunological qualities are determined by a single gene, while the morphological
polygenic, determined by multiple genes located on different loci.
Any system used in determining parentage (genetic marker) must ha ve three
characters:
Mendelian transmission;
Present at birth;
Lifetime Stability.
The chances of serological exclusion systems can be summarized as follow s:
System % chance
excluding
(Boorman K.,
et. al. 1985) % chance
excluding
(Knight B.,
et. al. 1991)
Systems of antigens-
erythrocyte
MNSs 32.1 32.1
Rh 28.0 28.0
Kidd 18.7 4.5
Duffy 18.3 4.8
ABO 17.6 17.6
Kell 4.5 3.3
Lutheran 3.7 3.3
Serum protein systems
GSC 30.2 14.5
Hp (haptoglobina) 18.1 17.5
PLG (plasminogen) 16.3 –
TF (transferina) 15.4 –
Pi ( α1-antitrypsin) 25.6 –
C3 – 14.2
Gm – 6.5
Erythrocyte enzyme
systems
PGM (fosfoglucomutase) 3.1 14.5
EAP (erythrocyte acid 23.4 21.0
200
phosphatase)
GLO (glioxilaza) 18.7 18.4
EsD (esteraza D) 9.7 9.0
ADA (adenozin deaminase) 4.5 4.5
AK (adenilatkinaza) 3.7 4.5
GPT
(glutamate pyruvate
transaminase) – 19.0
6-
fosfogluconatdehidrogenase
(6-GPD) – 2.5
Subtotal 1 93.3 93.0
HLA 90 90
Subtotal 2 99.6 99.0
AND
Total 99.9 99.9
Table no.1
The table above means that if it had tested 100 men who are fathers of children at
issue in 97 of them can be excluded – subtotal 1 – (HLA system by including a
conservative estimate gives a chance of exclusion of about 99 % – S ubtotal 2 -). With the
introduction of DNA typing can get a chance-total exclusion of 99.9%,.
Transmission characteristics of group ABO system:
Discovered by Landsteiner in 1901 (antigens A, B) added that the discove ry in
1902 AB. Erythrocyte Antigens occur from May 4th intrauterine lif e but anti-A antibody
titers and anti-B appears stable only at elevated 3-6 months after birth.
ABO phenotypes and their corresponding genotypes:
Table no.2
ABO characters are inherited through three allelic genes ca lled A, B and O. The
gene is considered a "silent" (moves) since it is erythrocyt e surface antigen and antiserum Phenotype Genotype
A AA
AO
B BB
BO
O OO
AB AB
201
that there is a highlight, it manifests itself phenotypically only if is a double dose from
both parents.
Each individual has a total of two chromosomes that carry alleles A, B or O, one
chromosome from each parent. ABO phenotype follows four groups: group A (phe notype
A: homozygous genotype AA-, AO-heterozygous genotype-), group B (phenotype B-BB-
BO), group A (phenotype O: OO-homozygous genotype-) and group AB (phenotype A B-
heterozygous genotype AB-).
Assuming that a parent group A (genotype AA may, AO) and the other i s group B
(genotype BB may, BO) are four possible combinations genotype AA x BB, AA x BO,
AO x BB, AO x BO.
AA x BB AB (obligatorily)
AA x BO AB, AO
AO x BB AB, BO
AO x BO AB, A, BO, OO
Table no.3
All possibilities resulting from a mixture of ABO groups are pr esented in the table below.
There are 10 combinations of parental phenotype resulting in 21 possible genotype
combinations, the combination that generates all the options is AO x BO.
Parents Children
Phenotype Genotype Genotype Phenotype
AxA AAxAA AA A și O
AAxAO AA și AO
AOxAO AA, AO și OO
AxB AAxBB AB A, B, AB, O
AAxBO AB și AO
AOxBB AB, BO
AOxBO AB, AO, BO, AB
AxAB AAxAB AA, AB A, B, AB
AOxAB AA, AB, AO, BO
AxO AAxOO AO A, O
AOxOO AO, OO
BxB BBxBB BB B, O
202
BBxBO BB, BO
BOxBO BB, BO, OO
BxAB BBxAB AB, BB A, B, AB
BOxAB AB, BB, AO, BO
BxO BBxOO BO B, O
BOxOO BO, OO
ABxAB AbxAB AA, AB, BB A, B, AB
ABxO ABxOO AOxBO A, B
OxO OOxOO OO O
Table no.4
It is not always possible to determine the genotypes listed in the table above.
An overview of the possibilities / impossibilities resulting show:
Parents Children
possibilities Groups
Impossible
OxO O A, B, AB
OxA O, A B, AB
OxB O, B A, AB
AxA O, A B, AB
AxB O, A, B, AB –
BxB O, B A, AB
OxAB A, B O, AB
AxAB A, B, AB O
BxAB A, B, AB O
ABxAB A, B, AB O
Table no.5
As a consequence of Bernstein's law stated above, children from g roup AB can t
come from two parents group 0, and each. May we add that the mother of a child can never
AB group A and vice versa, and the group did not even take the father in question (a
situation encountered in the exchange of children in maternity wards).
If we consider the subgroups A (A 1, A 2, A 3, A X, A end , A m, A el ), note that the
strongest are A1 and A2 (A1 holds between sites 800.000-900.000 attachment, A2 –
160.000-440.000 or A3 70.000-100.000, …, A el 100-400) in which the dominant A1 to A2,
both co-dominant trees to the B and O recessive to all three, add t he following
possibilities:
203
2nd parent First parent
Phen
otype genoti
p O A B AB Phenotype
OO AA AO BB BO AB Genotip
AB AB AO (A) AA (A)
BB (B) AO (A) AA (A)
BO (B) AB (AB) BO (B) AB (AB)
BB (B)
AB (AB) AB (AB) AB (AB)
B
BO
BB
OO (O)
BO (B) AO (A)
AB (AB) OO (O)
AO (A)
BO (B)
AB (AB) OO (O)
BO (B) AB (AB) BO (B)
AB (AB) BB (B)
A AO
AA OO (O)
AO (A) OO (O)
AO (A) AA (A)
O OO OO(O)
Table no.6
Group(Phenotype) genotip
A1 A1A1
A1O
A1A2
A2 A2A2
A2O
B BB
BO
O OO
A1B A1B
A2B A2B
Table no.7
Genotype possible Phenotype
possible children
A1A1 x BB A 1B
A1A1 x BO A 1B, A 1
A1O x BB A 1B, B
A1O x BO A 1, B, A 1, B, O
A1A2 x BB A 1B, A 2B
204
A1A2 x BO A 1,A 2, A 1B, A 2B
Table no.8
A2 antigen may occur in a child where one parent is phenotypic al ly A1 genotypic
ally if couples parenting are: either A1A2 x A 1O, fie A 1A2 x A 1A2, but not if the couple
Parental A1A1 x A 1A2.
Secretory system:
ABO blood groups can be detected not only on the erythrocyte surface a nd in
secretions (serum, saliva, gastric juices, ovarian cysts, semen, amniotic fluid and less in
sweat, urine, tears, bile and milk).
About 76% of the population is positive secretory: secret outside the quota
secretion of ABO blood group antigens and some specific substances. It was established
that the secretion of specific substances is controlled by a pai r of alleles is and. Sese
Individuals can be homozygous, and homozygous heterozogot Sese Sese. The al lele is
holding are secretive.
These people secrete two distinct substances mentioned secretions out side group ABO
antigens: an alcohol-soluble glycolipid (now the erythrocyte surfac e in almost all other
tissues but absent from the secretions) and a soluble glycoprotein (located in all
secretions). Thus secretory ABO groups were out in saliva antige ns A and B and H antigen
(secreted soluble glycoprotein in the mucous glands).
Sera containing anti-H agglutinins agglutinate group O red blood cells more
powerful, more poorly on the group A2, and the worse those of groups A1 and A1B;
In fact specific substances can be detected by specific and se nsitive to all men: even after
non-secretory show weak positive reactions elution techniques.
About 78% of the general population are Lewis negative (their genotype) , 22% +
Lewis (Le genotype). Lele and Sese genes segregates separate ly is that secretory number is
about the same as that of Lewis – (those who are not secret Lea + substances A, B, H).
Leb is not produced by a separate gene but result from the interacti on between
genes and Leah Lewis H. In fact, it is the group but not red cell levels, a nd if the amount of
antigens in serum is very high when an extra hand is fixed and er ythrocyte. Group
glycosophingolipids containing glycoprotein in plasma and secrete saliva.
Possible phenotypes are listed below, linked to the substances that ar e secreted in their
saliva every case.
205
Phenotype saliva Salivacontent Gene present
Le (a-b+): secretory H, Le b, little Le a H, Se, Le
Le (a+b-): unsecretory More Le a, at all Le b or
H,
little Le c H, se, Le
Le (a-b-): homozygous
lele , secretory H, at all Le a or Le b,
little Le c H, Se, le
Le (a-b-): homozygous
lele , unsecretory At all H, Le a and Le b,
little Le c H, se, le
Table no.9
There are anti-Lewis antibodies and anti-Leb Lea which usually oc cur together and
agglutinate erythrocytes, but not so much as to cause hemolysis in newborns.
Rh System:
Discovered in 1940 by Landsteiner and Wiener. They have immunized guinea pigs
and rabbits with blood from Maccacus Rhexus and obtained an antiserum to agglutinate
erythrocytes of Maccacus not only but also those of about 80-85% of the hum an
population of New York. So they realized they had discovered a new g roup of blood. Rh
antigens appear in the first month of intrauterine life, independent of other systems.
Aglutinele occur only through natural anti Rh isoimmunization (Rh-posit ive blood
transfusions from people Rh negative or Rh negative mothers immunized b y product
design tasks Rh positive).
Rh system has three pairs of allelic genes Cc, Dd, Ee on chromos ome 1: the locus
of a Dd alleles are located on the locus two alleles are locat ed on the locus three alleles Cc
and Ee.
Thus, on chromosome 1 is one member of each pair, one locus may be occupi ed by one or
other of the two allele pairs. The genotype is composed of two groups o f three antigenic
factors (inherited from the mother and father), which are sent in bulk.
Characters that are transmitted by Rh factors are:
• Antithetical nature which means that no factor other factors requir e the
presence of the same pair, the presence of one of the other factor s do not
exclude the presence of a pair (eg Cc);
206
• Alelomorf character whereby if a parent has a pair of both fa ctors, the
descendant is always forward only one of them;
• Every individual has at least one factor required in each pair ( so these factors
are transmitted from each parent equal).
It follows eight possible haplotypes: CDE, CDE, CDE, CDE, CDE, CDE , CDE,
CDE, 18 possible phenotypes and genotypes 36 (10 of which are negative: cde / cde /, cde
/ cde, cde / cde, cde / cde, cde / CDE, cde / cde, cde / cd e, cde / CoE, CoE / cde, CoE /
CoE). All variants of the D allele is Rh positive Rh (D) +, the remainder are Rh negative
(d) -.. All that were negative genotypes may induce the appearance of antibodies that are
stimulated with antigen anti.D D and must receive Rh negative blood or its genotype .
People Rh (D) + can be homozygous (D / D) or heterozygous (D / d), w hile those
Rh (d) – can only be homozygous (d / d).
Anti-Rh antibodies can destroy the antigens Rh (D).
Fig. No. 1
We can summarize the following:
• Antigen of a child (eg D) comes from one of the parents required;
• Two parents of a child required resulting Rh negative Rh negative;
• Resulting in two heterozygous parents heterozygous children;
• A child comes from a parent heterozygous CDE binding, otherwise the ac cused is
excluded;
• If the mother is deceased and the child in life is to exclude the defendant CC cc;
• If the mother and child are Rh + father has no chance of foreclosure on this system
because it can be DD or Dd.
207
MnSs System
The MN was identified by Landsteiner and Levine (1927), being their own man by
two genes and co-dominant trees alelomorfe MN. Antigens occur in t he ninth month of
intrauterine life, children aged 4-6 months with the same strength as adults.
Anti-M and anti-N occur through immunization and IgG antibodies are complete.
Group M appears in about 28% in group N at 22% and 50% in MN.
Transmission is by Mendel's laws, namely:
MM + MM = MM 100%
MM + NN = MN 100%
MM + MN = MM 50% + MN 50%
MN +MN = MM 25% + MN 50% + NN 25%
Were found not only extremely rare and unimportant to the antigen
isoimmunization M, N or posttransfuzional newborn.
Later, Walsh and Montgomery (1947) identifies the system Ss S alle le is dominant
and recessive allele s is. MN and Ss loci adjacent positions on chromosome 4 and ther efore
be transmitted together.
Ss-type antibodies are only immune from occurring consecutive trans fusions or
tasks. They are incomplete IgG-type antibodies. There genotypes SS , Ss and ss with a
phenotypic frequency of 11%, 44% and 45%. Unlike anti-M and anti-N, anti-S and anti-s
were active at 37 degrees C agglutinate erythrocytes in 55% ( anti-S) and 89% (anti-s) and
are responsible for both events postransfuzionale hemolytic and after birth.
Genotypes and phenotypes MNSs system:
Anti-M Anti-N Anti-S Anti-s Phenotype Genotype
+ – + + MSs MSMs
+ – + – MS MSMS
+ – – + Ms MsMs
+ + + + MNSs MSNs
MsNS
+ + + – MNS MSNS
+ + – + MNs MsNs
208
– + + + NSs NSNs
– + + – NS NSNS
– + – + Ns NsNs
Table no.10
Antigens MN, Ss have a significant poliformism race. Thus, there are complex
genes: MS, Ms, NS, Ns. MNSs system is considered most effect ive in the expertise of
parenthood.
We can summarize by:
• If both parents are homozygous for the same result as only children of the same
homozygous;
• If both parents are heterozygous for the accused no chance of exclusion;
• MN accused have no chance of exclusion;
• M and N antigens can not occur in a child if there is at least one parent;
• If a child is NN (MM) and NN parents, father MM MN exclude (ie NN);
Mother – MM (or NN) NN can not have a child (ie MM) phenotype rega rdless of the
father.
Differentiation in determining blood groups by race
1. There are at least four forms of hemoglobin:
– Hemoglobin A (normal type of adult white)
– F (fetal type)
– S (10-15% of adult black)
– C (3% of adult black)
There is pathological form (homozygous SS sickle cell disease pr esent). The characteristic
shape S is recessive to A that it is not possible to differentia te between A and AS usual.
Kell antigens are found only in white, while 90% of Duffy antigens West African blac ks.
Animals have their own blood type, different from human.
2. Duffy system for the Negroid race (see above) and other populations.
Immunization response to blood group antigens
The antigenic proteins are considered as A, B, Rh.
Rh immunization:
209
Following administration of blood:
• The first administration of about 500 ml of Rh positive blood to an Rh
negative person with 50% probability of inducing isoimmunization in
the next 2-6 months.
• About one third of the Rh negative but are "resistant" (non-accountable)
and can not form anti-D antibodies. Others, however, although there
were still detectable antibodies form immune, which could prove the
presence of hemolytic disease from their new born.
Pregnancy:
• Isoimmunization is a natural method that produces anti-D highlighted at
the end of birth to about 2% of the mothers while the Rh positive fetus
during pregnancy bleeding.
• At about 6 months after birth rate of detection of antibodies raised t o
7% of the mothers (explanation consists in passing the maternal
circulation of quantities of fetal blood – usually about 10 ml – when
transplacental bleeding) as the fetal blood passes much larger quanti ty
will be more intense immune response (IgM initially and then with
IgG). amniocentesis, caesarean manual removal of placenta and
increase the risk of anti-D concentration at the second birth but e ven
small amounts of fetal blood may initiate an intense immune respons e
with production of haemolytic disease of newborn.
• In a surprise when there is blood group incompatibility between mother
and fetus Rh-Rh +, Rh immunization in pregnancy is less apt to occur.
ABO immunization:
• The ABO system in contrast to the Rh system, anti-A and anti-B are usually
present in inverse relation to the presence of serum erythrocyte antigen.
• There is even a small amount of antibodies developed by immunization
counterparts as a result of entering into service during the life bl ood group
antigens A, B, H, on various occasions (the blood of others, microorganism s,
intestinal flora, dust particles, etc.). that first appears to be produced
cvasiconstant immunization (IgM response).
• Response to administration of incompatible blood incomplete development of
IgG from day 2-3 with a maximum on day 10-14 and then a slow decline to da y
210
20. To this is added the hemolizine detection. The latter proves a rec ent
immunization. The main problem is differentiating hemolytic immuniza tion
natural immunization, which can be made with pig erythrocytes have called
Rev-like antigens which agglutinate with anti-A IgG hemolici and not natural
anti-A IgM.
HLA system lymphoma
In the major histocompatibility complex, HLA system is the most comprehensive
system of human antigens, especially as it is present on all nucl eated cells, platelets and
even sperm. Histocompatibility antigens are defined as antigens ca using immunological
reaction to the transfusion or organ transplant between two different organisms genetically.
MHC genes belonging to the immunoglobulin gene family, involved in re cognition of both
their structures and of the foreign body. The proteins encoded by the m have great
complexity of biological attributes, genetic individualization of t heir responsibility of each
person is of paramount importance.
HLA system is encoded by genes located on the short arm of chromosom e 6. Each
locus can be occupied by several alleles. At the level of the chr omosome genes HLA-A, B,
C and D are well-defined locations. Thus: HLA-D region encoded mole cules located the
centromeres of class II and has three loci called DP, DQ and D R. Towards the end regions
are telemeric ă HLA-A, B and C, which encodes class I molecules are most polym orphic
regions
HLA-A and HLA-B haplotypes 23 and 49 respectively.
A haplotype is a set of genes located on a chromosome that are unique genotypic
expression. Between HLA-D and HLA-B genes coding for molecules loc ated class III, ie
two, C II, C IV, and factor B of complement.
HLA antigens are genetic transmission of Mendelian laws of tr ansmission co-
dominant trees on the system. Multitude of antigens located on each locus and their
immense possibilities of combining the haplotypes of this system ex plains the extreme
polymorphism of antigens, unmatched by any other human genetic system.
For serological HLA typing using various techniques, the method being used
limfotoxicit ății in the presence of rabbit complement. For each antigen are used t o
establish several test sera. Study of HLA antigens A, B and C (class I) requires peripheral
blood lymphocytes, and to highlight the antigens HLA-DR, DP and DQ (Cla ss II) shall be
used only in peripheral blood B lymphocytes.
211
For class II HLA antigens printed in the molecular biology technique s are used:
RFLP, PCR, PCR-RFLP (the last consisting of the combination of me thods mentioned
above, based on the characterization of fragment length polymorphism af ter amplification
of restriction variable region).
Serologically HLA antigens are clearly differentiated from e ach other. However,
some of them have similarities probably due to similar molecular structures, which can
lead to cross reactions. For example, a relatively strong cross- reactivity between antigens
HLA-A2 and A28, between the A1, A3 and A11, between the A9 and A10 and betw een
A19-complex topics (A29, A30, A31, A32, A33).
With regard to biological and clinical value of HLA system, it is particularly in
organ transplantation, bone marrow in haematological disorders, transfusi ons and expertise
in the issues of parenthood.
Thus, the HLA system is the most important genetic marker. So f ar not identified
any other system of genetic markers have such a genetic polymorphism in a pa ttern so well
defined.Also, the HLA system is very useful in human genetic studies , studies of evolution
and selection of genetic mechanisms, the characterization of human popul ations, the
composition of chromosome maps in the study and the study of diseases associated with
heredity.
212
References
1. Baum GL at al. Baum”s Textbook of Pulmonary Diseases. 7 th ed. Phil adelphia
(USA): Lippincott Wiliams & Wilkins Publishers; 2003.
2. Becker RF Criminal Investigation. 3 rd ed. Sudburz *USA(: Jones & Bartlett Publishers;
2008.
3. Behera A, Das S, Das GS. Eye is the Spy of Forensic. Medicine. J Indian Acad
Forensic Med.2003; 25 (4):165-167.
4. Beli ș V. „Investiga ția microscopic ă în medicina legal ă” – Editura Academiei,
Bucure ști, 1993.
5. Beli ș V. „Tratat de medicin ă legal ă” – Editura Medical ă, Bucure ști, 1995
6. Beli ș V., Florian Șt., Mihalache G. –„Medicin ă legal ă” – Editura Treira, Oradea, 1999
7. Beli ș V., Nane ș Constan ța – „Traumatologia mecanic ă în practica medico-legal ă și
judiciar ă” – Editura Academiei, Bucure ști, 1985
8. Brooker C, Nicol M.Nursing Adults: The Practice of Caring. 1 st ed. Edinburgh (UK):
Mosby; 2003.
9. Cheng et.al. Supplementary tests for conformation of brain death. Uni v. Sci B 2008
9(11): 921-922.
10. Curc ă. C.” Medicina Legal ă Curs”, Bucure ști, 2005
11. Dermengiu, D.”Patologie medico –legal ă”, Ed.Via ța Medical ă Româneasc ă, Bucure ști,
2002.
12. Diaconescu G. „Infrac țiunile în legi speciale și legi extrapenale” Editura ALL,
Bucure ști
13. Dickshit PC. Textbook of Forensic Medicine and Toxicology. New Delhi ( India):
PeePee Publishers; 2007.
14. DiMaio VJM, Dana SE. Handbook of Forensic Pathology. Austin (USA): Lande s
Bioscience; 1998.
15. DiMaio VJM. Gunshot Wounds Practical Aspects of Firearms, Ballisttics, and F orensic
Techniques. 2 ad ed. Boca Raton (USA): CRC Press; 1999.
16. DiMaio VJM, DiMaio D. Forensic Pathology, 2nded. Boca Raton (USA): CRC Press;
2001.
17. Dolinak D, Matshes EW, Lew EO. Forensic pathology. 1 st ed. Burlington (USA):
Elsevier Academic Ores; 2005.
18. Dog ăroiu C., Dermengiu D., Curc ă C.- Essentials of Forensic Medicine, Ed Tehnoplast
Company SRL, Bucure ști, 2010
19. Dragomirescu V.T. „Problematica și metodologia medico-legal ă” – Editura Medical ă,
Bucure ști, 1980
20. Dressler M. „Etic ă, deontologie și drept medical” – Timi șoara, 1998
21. Dressler M. „Medicin ă legal ă” – Timi șoara, 1985
22. Frizzell JP, et al. Handbook of Pathopsysiology. Pennsylvania (USA): Springhouse
Corporation; 2001.
23. Ford MD et al. Clinical Toxicology. 1 st ed. Phialdelphia (USA): W.B . Saunders Co;
2001.
24. Green MA. Postmortem changes in Encyclopedia of Forensic Scie nces. London (UK):
Academic Press; 2000.
25. Guharaj PV, Chandran MR. Forensic Medicine, 2 nd ed. Hyderabad (India): Orient
Longman; 2003.
213
26. Gwinnell E, Adamec C. The Encyclopedia of Drug Abuse. 1 st ed.new York (USA):
Facts on File; 2008.
27. Heard BJ. Handbook of Firearms and Ballistics. 2 nd ed. Chichester (UK): Wiley
Interscience; 2008.
28. Houck MM. Forensic Science: Modern Methods of Solving Crime. West Port (USA):
Praeger; 2007.
29. Hueske EE. Practical Analysis and Reconstruction of Sooting Incident s. Boca Raton
(USA): CRC Press; 2006.
30. Knight B. Forensic Pathology. 2 nd ed. New York (USA): Oxfort University Press;
1996.
31. Knight B. Simpson’ s Forensic Medicine, 11 th ed. Londo(UK): Hodder Arnold
Publication; 1997.
32. Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of Emergency Medicine.
3rd ed.new York (USA): McGraw/Hill; 2010.
33. Kumar V, Abbas AK, Fausto N, Mitchell R. Robbins Basic Pathology. 8th ed. London
(UK): Elsevier; 2007.
34. Lerner AJ. Diagnositc Criteria in Neurology (Current Clinical Neurology). 1 st ed. New
York (USA): Humana Press; 2006.
35. Lerner KL, Lerner BW, editors. World of Forensic Science. Farmingt on Hills (USA):
Thomson Gale; 2006.
36. Madea B, Tsokos M, Preub J. Death Due to Hypothermia. Morphological F indings,
their Pathogenesis and Diagnostic Value in Forensic Pathology Revie ws Volume 5 by
Michael Tsokos, Humana Press; 2008.
37. Mason JK. Forensic Medicine for Lawyers. 3 rd ed. London (UK): Butter/Worths; 1995.
38. Mayer R. Embalming: History, Theory, and Practice. 4 th ed. New York (USA):
McGraw/Hill Medical; 2005.
39. Meyers DW. The Human Body and the Law. 2 nd ed. New Jersey (USA): Stanford
Univ. Press; 2006.
40. Mihalache G., Buha ș C. „Compendiu de medicin ă legal ă pentru medici generali ști și
stomatologi” ,Editura Univ. Oradea, 2007
41. Mohandas A, Chow SN. Brain death: a clinical and pathological study. J. Neurosurg.
35: 211, 1971.
42. Molina DK. Handbook of Forensic toxicology for medial examiners. Boca ra ton
(USA): CRC Press; 2010.
43. Moraru I. „Anatomie patologic ă”, Editura Medical ă, Bucure ști, 1980
44. Mostofi SB. Fracture Classifications in Clinical Practice. London (UK): Springer;
2006.
45. Narayan Reddy KS- The Essentials of Forensic Medicine And Toxic ology, K Suguna
Devi, Nineteenth Edition , 2000.
46. Nica C-tin. – „Urgen țe chirurgicale” – Vol I și II, Editura Mitron, Timi șoara, 1999
47. Oehmichen M, Auer RN, Konig HG: Forensic neuropathology and associate d
neurology. 1 st ed. Berlin (Germany): Springer; 2009.
48. Pollak S, Saukko P. Gunshot wounds. in Siegel J, Knupfer G, Saukko P. Encyclopedi a
of Forensic Sciences. Burlington (USA): Academic Press; 2000.
49. Pollard BJ. Handbook of Clinical Anaesthesia. 2 nd ed. Edinburgh (UK): Churchill
Livingstone; 2004.
50. Posner JB, Saper CB, schiff N, Plum F. Plum and Posner’s Diagnosis of Stupor and
Coma. 4th ed. New York (USA): Oxford University Press; 2007.
51. Quai I., Terbancea M. „Introducere în teoria și practica medico-legal ă”, Editura Dacia,
Cluj-Napoca, 1978.
214
52. Rao NJ. Textbook of Forensic Medicine and Toxicology. 1 st ed. New Delhi (India):
Jaypee Brothers Medicale Publishers; 2006.
53. Rastegar DA, Fingerhood MI. Addiction Medicine: An Evidence-Based H andbook. 1 st
Philadelphia (USA): Lippincott Williams & Wilkins; 2005.
54. Rich R, Dean DE, Powers RH. Forensic Medicine of the Lower Extr emity. Human
Identification and Trauma Analysis of the Thigh, Leg, and Foot. Totowa USA):
Humana Press; 2005.
55. Rohkamm R, Color Atlas of Neurology. Stuttgart (Germany): Theime: 2004.
56. Rosenberg RN, Consciousness, Coma, and Brain Death JAMA 2009 301 11 1172 /
1174.
57. Russel RCG, Wiliams NS, Bulstrode Ccjk. Bailey & Love’s Short Practice of Surgery.
24 th ed. London (UK): Hodder Arnold Publication; 2004.
58. Savino JO, Turvey BE. Rape Investigation Handbook. London (UK): Elsevier; 2005.
59. Savitz SI, Caplan LR Vertebrobasilar Disease current concepts N Engl J Med 2005;
352: 2618 – 2626.
60. Scanlon VC, Sanders T. Essential of Anatomy and Physiology 5 th ed. Philadelphia
(USA) F.A. Davis Company, 2007.
61. Scripcaru C., B. Ioan- Forensic Medicine for students, Ed. Junimea, Ia și, 1999.
62. Scripcaru Gh., Terbancea M. „Patologie medico-legal ă” – Editura Didactic ă și
Pedagogic ă, Bucure ști, 1983.
63. Scripcaru Gh., Ciornea T., Ianovici N. „Medicin ă și drept” – Editura Junimea, ia și,
1979
64. Sedgwick K, Medical Examiners’ and Coroners’ Handbook on Death Registr ation and
Fetal Death Reporting. Maryland (USA): DHHS Publication; 2003.
65. Siegel J, Knupfer G, Saukko P. Encyclopedia of Forensic Sciences. New York (USA):
Academic Press; 2000.
66. Stark MM. A Physician’s Guide to Clinical Forensic Medicine. New Jersey (USA):
Humana Press: 2000.
67. Suzuki O, Watanabe K. Drugs and Poisons in Humans. A Handbook of Practical
Analysis. Berlin (Germany): Springer; 2005.
68. Tsokos M (editor) Forensic Pathology Reviews, vol. 1 New Jersey (US A): Humana
Press; 2004.
69. Turk EE. Fatal Falls from Height in Forensic Pathology Reviews Volume 5 b y Michael
Tsokos, Humana Press; 2008.
70. Underwood JCE. General and Systemic Pathology. 4 th ed. London (UK): Elsevier;
2007.
71. U.S. Department of Health and Human Services, Centers for Disease Control and
Prevention, National Center for Health Statistics. Instructions f or Completing the
Cause/of/Death Section of the Death Certificate. August 200 404/0377 (8/04).
72. Victor M, Ropper AH, Adams RD. Adams & Victor’s Principles Of N eurology. 7 th ed.
Philadelphia (USA): CRC Press, 2009.
73. Wagner SA. Death Scene Investigation: A. Filed Guide. Boca Raton ( USA): CRC
Press, 2009.
74. Wecht CH, The History of Legal Medicine. J Am Acad Psychiatry Law 2005 33:245-
51.
75. Whitfield PC et. Al. Head Injury. A Multidisciplinary Approach Cam bridge (UK):
Cambridge University Press; 2009.
76. Wick R, Byard RW. Electrocution and the Autopsy in Forensic Pathology R eviews
Volume 5 by Michael Tsokos Humana Press; 2008.
215
77. Wijdicks EFM.The diagnosis of brain death N Engl J Med, Vol. 344, No 16 2001
1215-1221.
78. Youngner SJ, Arnold RM, Schapiro R. The Definiton of Death: Contemporary
Controversies. 1 st ed. Baltimore (USA): Johns Hopkins University Press; 2002.
79. Dental Dictionary: LeFort Fracture [Online] 2010 [cited 2010' Feb 25] Available from:
URL: http://www.answers.com/topic/lefort-fracture
80. Index of /images/2/2f [Online] 2008 Feb 17 [cited 2010 Feb 26] Available from: URL:
http://wikidoc.org/images/2/2f/Osborne example.jpg
81. LSD Drug Pictures [Online] 2002 [cited 2010 Mar 18] Available from: URL:
http://www.drug-rehabs.org/lsd-drug-pictures.php
Copyright Notice
© Licențiada.org respectă drepturile de proprietate intelectuală și așteaptă ca toți utilizatorii să facă același lucru. Dacă consideri că un conținut de pe site încalcă drepturile tale de autor, te rugăm să trimiți o notificare DMCA.
Acest articol: C2 Forensic Medicine [608266] (ID: 608266)
Dacă considerați că acest conținut vă încalcă drepturile de autor, vă rugăm să depuneți o cerere pe pagina noastră Copyright Takedown.