Dark Side: Some Kind of Justice From Behind The Grave
Some
pathologists, usually those not normally concerned with criminal and litigious
cases, claim that an autopsy report should be a bare recitation of the physical
findings, with no discussion or interpretation of the significance of those
findings. This is an abdication of the pathologist's responsibility because,
especially in criminal deaths, it is these condusions that are of most interest
and use to che investigating officers, lawyers and courts. After the detailed
description of the external and internal appearances, a short resume should be
offered of the major positive findings and their relationship to the cause of death.
In many cases this will be obvious, as in a gunshot wound of the head. Matters
such as the probable type of weapon, the range, the direction and the likely
rapidity of death, however, should also be discussed. When the findings are
less clear cut, or are multiple, then the alternatives should be discussed,
giving a differential diagnosis of the cause of death and detailing the
possible sequence of events. If it is possible, a ranking order of probability
of the various alternatives can be offered. Time of death and the limitations
of accuracy in this particular case should be set out when the issue is
relevant to the investigation.
What
is really required is as full an interpretation as possible, without venturing
into the undesirable fields of unwarranted speculation or overinterpretation,
whch was the bane of forensic pathology in former years and is still practised
too much even today, to the detriment of the good reputation of the speciality
Eye
signs include loss of the corneal and light reflexes leading to insensitive corneas and light
reflexes unreactive pupils. Though the iris responds to chemical stimulation
for hours after somatic death, the light reflex is lost as soon as the
brainstem nuclei suffer ischaemic failure. The pupils usually assume a middilated
position, which is the relaxed neutral position of the pupillary muscle, though
they may later alter as a result of rigor. There may be a marked difference in
the degree of dilatation of each pupil,
but this has no significance as a
diagnostic sign either of a brain lesion or of drug intoxication. In conditions such as
morphine poisoning, where the pupils may
be contracted during life, dearh may
allow this to persist or the pupils may dilate
to the 'cadaveric position'.
In
addidtion to irregular size, the pupils may loose their circular shape after
death as a result of uneven relaxation. This
is usually easy to differentiate from the more obvious
irregularity caused by ante-mortem abnormality of the iris. The eye globe
tension decreases rapidly, as it is dependent upon arterial pressure for its
maintenance. The eyeball feels progressively softer within minutes and the
cornea soon loses its normal glistening reflectivity because of laxity and
failure of lachrymal moistening.
The
eyelids usually close, but this is commonly incomplete, the flaccid muscles failing to the full
occlusion that occurs in voluntary
closure: Where the sclera remains
exposed, two yellow triangles of desiccated discoloration appear on each side of the
cornea within a few hours, becoming brown and then sometimes almost black,
giving rise to the name 'tache noire'. When viewed with an ophthalmoscope, the
retina provides one of the earliest positive signs of death. This is the well
known 'trucking' of blood in the retinal vessels, when loss of blood pressure
allows the blood to break up into segments, similar to trucks in a railway train.
This phenomenon occurs all over the body, but only in the retina is it
accessible to direct viewing.
Post-mortem
change in the eye, the so-called tache noire
The
test is not easy to carry out, as the retina of a corpse seems far more
difficult to visualize than in a living person. Many observers have described
the agonal and early post-mortem appearances of the retina, though some of
their accounts are rather contradictory and of little practical value,
especially when they attempt tn llse them to estimate the time since death. One
of the best investigations into the phenomenon was by Wroblewski and Ellis
(1970), who studied retinal and corneal changes at dearh in 300 patients. About
a third of the total exhibited trucking, most of them within an hour of death. Part
of the difficulty in examining the remainder was that clouding of the cornea
occurred in 75 per cent of patients within 2 hours of death. They concluded
that segmentation was a purely post-mortem change and any intravascular movement
of blood, however irregular, was an indication for continued resuscitation.
Confusion
often arises about the distinction between the mode of death and its cause. This
is particularly important in relation to the documentary certification of
deaths, but the same confusion sometimes occurs among pathologists, especially
those who are not habitually involved in medicolegal cases. The mode of death
refers to an abnormal physiological state that pertained at the time of death:
for example, 'coma', 'congestive cardiac failure', 'cardiac arrest' and
'pulmonary oedema'. These offer no information as to the underlying pathological
condition and should not be used as the definitive
cause of death unless further qualified by the more fundamental aetiological
process.
To the forensic pathologist a number of post-mortem changes are of interest and potential usellness, mainly in relation to the estimation of the post-mortem interval, possible interference with the body, and an indication of the cause of death. Post-mortem hypostasis is known under a variety of older names, such as 'lucidity', 'staining' or 'cogitation', but the current title is most suitable as it indicates the cause. Hypostasis occurs when the circulation ceases, as arterial propulsion and venous return then fail to keep blood moving through the capillary bed, and the associated small afferent and efferent vessels. Gravity then acts upon the now stagnant blood and pulls it down to the lowest accessible areas. The red cells are most affected, sedimenting through the lax network, but plasma also drifts downwards to a lesser extent, causing an eventual post-mortem 'dependent oedema', which contributes to the skin blistering that is part of early post-mortem decay. The arrival of erythrocytes in the lower areas is visible through the skin as a bluish red discoloration, 'hypostasis'. It often begins as blotchy patches on both lateral and dependent surfaces, but also on the upper surfaces of the legs, especially thighs. These soon coalesce and slide down to the lowest areas.
The
pattern of hypostasis depends on the posture of the body after death. It is
most common when the deceased body is lying on its back, with the shoulders,
buttocks and calves pressed against the supporting surface. When the body lies
for a sufficient time on the side or face, the hypostasis will distribute
itself accordingly, again with white pressure areas at the zones of support.If
the body remains vertical afier death, as in hanging, hypostasis will be most
marked in the feet, legs and to lesser extent in the hands and distal part of
the arms. In additionto pallor of the supporting areas, any local pressure can exclude
hypostasis and produce a distinct pattern in contrastto the discoloured area.
Examples include the irregular linear marks made by folds in rumpled
bedlinen, the pattern of fabric from coarse cloth, the pressure of tight belts,
brassitre straps, pants' elastic and even socks.
The usual hue is a bluish red, but variation is wide. This depends partly on the state of oxygenation at death, those dying in a congested, hypoxic state having a darker tint as a result of reduced haemoglobin in the skin vessels. This isan unsure indicator of the mode of death, however, and no reliance can be placed on a cyanotic darkening of the hypostasis to indicate a hypoxic death in the sense of 'asphyxia'. Many natural deaths from coronary or other disease have markedly dark hypostasis. Often the colour of the hypostasis varies from area to area on the same body. Sometimes a rim of lighter colour may be seen along the margin of the lower darker area and sometimes there is a definite contrast between a bluish zone and a pink margin. This may appear and change as the post-mortem interval lengthens. Often the whole area of hypostasis is pink or bright red. When death has been due to hypothermia or exposure to cold in the agonal period, such as drowning, the colour may assist in confirming the cause of death; again this is relatively non-specific because bodies exposed to cold after death (especially in mortuary refrigeration) may turn pink after an initial stage of normal bluish-red tint.
Once
hypostasis is established, there is controversy about its ability to undergo
subsequent gravitational shift. If the body is moved into a different posture,
the primary hypostasis may either:
Ø -
remain fixed
Ø -
move completely to the newly dependent zones or
Ø -be
partly fixed and partly relocated.
Thus if a corpse is found with the hypostasis in an obviously inappropriate distribution related to the present posture, it must have been moved after death.
Just
as blood settles in dependent skin, so it does in other tissues and organs. The importance in forensic
autopsy work is the differentiation of organ hypostasis from ante-mortem lesions.
In the intestine, dependent loops of jejunum and ileum may be markedly
discoloured and mislead the inexperienced pathologist into suspecting
mesenteric infarction or strangulation. This hypostasis is discontinuous,
however, revealing interrupted segments when the gut is laid out. Often loops
in the pelvis are worst affected, because of their lower position. The lungs
almost always show a marked difference in colour from front to back, the
anterior margins being pale and the posterior edges lying in the paravertebral
gutters being dark blue. This is often accompanied by an obvious difference in
fluid content, congestion and oedema being more marked posteriorly. The myocardium
often shows a dark patch in the posterior wall of the left ventricle that must
not be mistaken for early infarction.
Fresh
bruises may also be swollen and slightly raised above the surface. If a
post-mortem pressure mark (such as from a belt or tight clothing) crosses an
area of hypostasis, there will be a pale bloodless zone, but a bruise will not
be affected. Hypostasis is in the most superficial layer of the dermis and any
exuded blood can be wiped or washed away from the incised surface. A bruise is
often deeper in the skin or underlying tissues and is fmed, being infiltrated
through the tissues outside the ruptured vessels. An exception is intradermal bruising,
but this is usually patterned or linear and rarely can be confused with
hypostasis. Histological examination may be necessary finally to decide the
matter.
Rigor
mortis unlike hypostasis, the stiffening of the muscles after dearh has some
relevance in determining the post-mortem interval. It has been known since
antiquiry that immediately after death there is general muscular flaccidity,
usually followed by a period of partial or total rigidity, which in turn passes
off as the signs of decomposition appear. The timing of this sequence of events
is so variable, however, that it is a poor indicator of the time since death.
There
has been some controversy over whether rigor only stiffens the muscles or
actually shortens them. Sommer, as long ago as 1833, claimed that muscles
contracted after death and the changes were actually known as 'Sommer's movements'.
There seems to be no doubt that some shortening does occur, but the noticeable
effects are slight because both flexor and extensor muscle groups oppose each
other across most limb joints. When fully established, rigor is 'broken' by
forcible movements of the limbs or neck, then it will not return, a phenomenon
utilized daily by mortuary staff and undertakers when preparing a body for a
coffin. If rigor is still developing, it will continue in the new posture of
the limbs after they have been stretched. 'Breaking' fully established rigor isan
accurate description, as the rigid, inelastic fibres are physically ruptured
-sometimes tearing the muscle insertionsfrom the bone. Rarely, rigor can assist
in showing that a body has been moved between death and discovery. If an arm or
leg is found projecting into free space without support, in a posture that
obviously could not have been maintained during primary post-mortem flaccidity,
then it must have been rolled over or otherwise moved.
It
was shown in the earlier section on the biochemistry of rigor that marked
depletion of glycogen stores in the muscle by violent exertion immediately
before death can hasten the onset of muscular rigidity. Most cases of cadaveric
spasm occur in similar circumstances and it was said to be particlarly common
on the battlefield amongst soldiers slain in combat. In the civilian sphere it
is most often seen in persons who fall into water or drop some distance down a
precipitous slope such as a cliff. They may clutch at some nearby object, such
as grass or shrubs, in an effort to break their fall and such material may be
found held tightly in their fingers, even when the body is examined within a
few minutes. Another possibility, more common in detective fiction than in
practice, is the gripping of a pistol with the fingerstill tightly flexed on
the trigger, as evidence of true suicide rather than a 'planted' weapon in a
homicide where an attempt has been made to simulate self-shooting. Thechances
of this actually being encountered by a pathologist are less than once in
several professional lifetimes. If found in the victim of drowning, or of a
slide from a height, it has some value in confirming that the person was alive
at the time of the fall, thus excluding the post-mortem disposal of an already
dead body. Of course the body must be examined before ordinary rigor might be
expected to have developed, or the presence of cadaveric spasm cannot then be
assumed.
The
usual process of corruption of the dead body begins at a variable time after
death, but in an average temperate climate may be expected to begin at about 3
days in the unrefrigerated corpse. Even in temperate zones there can be a wide
range of ambient temperatures, from below freezing to near blood heat. In the
tropics, far higher temperatures are commonplace, but in high latitudes or
elevations, deep-freeze conditions can keep decomposition at bay indefinitely,
as in the case of modern discoveries of prehistoric mammoths and medieval
Esquimaux. It is therefore futile to attempt to construct a timetable for the
stages of decomposition, except to point out salient markers for an undisturbed
body in an 'average' indoor environment of about 18°C in temperate climates.
From this approximate baseline the pathologist must then extrapolate for local
variations appropriate to his climatic and geographical condition.
Whatever
the time scale, the general order of corruption is similar, though the degree
of advancement may vary between different areas-of even the same corpse. Usually
the first external naked-eye sign is discoloration of the lower abdominal wall,
most often in the right iliac fossa where the bacteria-laden caecum lies fairly
superficially. Direct spread of organisms from the bowel into the tissues of
the abdominal wall breaks down haemoglobin into sulphaemoglobin and other
pigmented substances. This discoloration spreads progressively over the abdomen,
which in the later phase begins to become distended with gas.
Marine
predation in a body after 3 months in the North Sea. The victim was fiom an oil
rig and hadfloatedon the surface in a life jacket. Much of the skin has been
removed by crustaceans.
The
usual posture of a freely floating body is face down, as the head is relatively
dense, and does notdevelop the early gas formation in the abdomen and thorax. This
lower position favours fluid gravitation and hence more marked decomposition,
so that the face is often badly putrefied in an immersed body, making visual
recognition dificult or impossible at an early stage. As stated, temperature is
the major determinant of the rate of putrefaction.
The
rate of decay of bodies buried in earth is much slower than of those in either
air or water. In fact the process of putrefaction may be arrested to a
remarkable degree in certain conditions, allowing exhumations several years
later to be of considerable value. In
this respect the prospect of an exhumation should never be dismissed on the
grounds that because of the lapse of time, it is bound to be worthless. It may
turn out to be of little value, but this cannot be anticipated, and not
infrequently the condition of the body may be surprisingly good.
The
speed and extent of decay in interred corpses depends on a number of factors.
If the body is buried soon after death, before the usual process of decay in
air begins, putrefaction
is less and may never proceed to the liquefying corruption usually inevitable
on the surface. A lower temperature,
exclusion of animal and insect predators, and lack of oxygen are important
factors. Although most bacteria originate in the intestine, there is less
access for secondary invaders and the restriction of oxygen inhibits aerobic
organisms. If the body is
rotting before burial then, although the process slows down, it will still
severely damage the corpse, as enzymatic and bacterial growth have had initial
encouragement
from a higher ambient temperature and free access of air.
When
bodies are buried in coffins in vaults, rather than in earth, then again there
can be a variable rate of decay. Some bodies may develop adipocere, others may
wholly or partly mummify.
The
most common chemical estimation performed on thevitreous fluid in the context
of the post-mortem interval is that of potassium. There is a marked and
progressive rise in the potassium concentration after death, the controversy revolving
around whether this rise is simply linear or whether it is biphasic. The degree
of confidence is also in dispute and the effect of variable factors is another
contentious matter.
First,
the potassium values from either eye often differ, sometimes by a considerable
amount. The sampling methods are then critical, as small or marginal samples
vary greatly; if aspiration is forcible or from too near the retina, cellular
fragments distort the values, because the potassium reaches the vitreous by
leaching out from the retina. The effect of temperature changes post-mortem is
also undoubtedly important. In addition, different analytical techniques used
to estimate the potassium give different results, the older flame photometric methods
producing a different range of values compared with modern selective-electrode
procedures.
To
conclude the crime scene presents a large amount of information about the perpetrator’s actions. In order for the
classification and linking of serial murderers’
offenses to be more than educated guesswork, conclusions must be based on
empirical research of consistencies in criminal behavior and the relationship
of those actions to aspects of an offender that are available to the police in
an investigation. Therefore, a model of any violent crime, especially that of
serial murder, should be built on the central hypothesis that offenders differ
in their actions when committing crimes and that these differences reflect
different interactions between the offender and victim. However, most published
literature on variations in serial murderers’ behaviors have neglected
victim/offender interpersonal actions that occur duringa crime. Rather,
research has tended to combine accounts of crime scene actions with
explanations of motivations, intentions, personality attributes, and other
inferred offender characteristics.
Acknowledgements:
www.politie.nl Politiekorpschef @Janny Knol©
www.aived.nl AIVD – @Erik Akerboom ©
www.politie.nl WEB Politie - @Henk van Essen©
https://www.police-nationale.interieur.gouv.fr/ @ Stephane Folcher ©
Bibliography:
1. Criminal Investigations – Crime Scene Investigation.2000
2. Forensic Science.2006
3. Techniques of Crime Scene Investigation.2012
4. Forensics Pathology.2001
5. Pathology.2005
6. Forensic DNA Technology (Lewis Publishers,New York, 1991).
7. The Examination and Typing of Bloodstains in the Crime Laboratory (U.S. Department of Justice, Washington, D.C., 1971).
8. „A Short History of the Polymerase Chain Reaction". PCR Protocols. Methods in Molecular Biology.
9. Molecular Cloning: A Laboratory Manual (3rd ed.). Cold Spring Harbor,N.Y.: Cold Spring Harbor Laboratory Press.2001
10. "Antibodies as Thermolabile Switches: High Temperature Triggering for the Polymerase Chain Reaction". Bio/Technology.1994
11. Forensic Science Handbook, vol. III (Regents/Prentice Hall, Englewood Cliffs, NJ, 1993).
12. "Thermostable DNA Polymerases for a Wide Spectrum of Applications: Comparison of a Robust Hybrid TopoTaq to other enzymes". In Kieleczawa J. DNA Sequencing II: Optimizing Preparation and Cleanup. Jones and Bartlett. 2006
13. Nielsen B, et al., Acute and adaptive responses in humans to exercise in a warm, humid environment, Eur J Physiol 1997
14. Molnar GW, Survival of hypothermia by men immersed in the ocean. JAMA 1946
15. Paton BC, Accidental hypothermia. Pharmacol Ther 1983
16. Simpson K, Exposure to cold-starvation and neglect, in Simpson K (Ed): Modem Trends in Forensic Medicine. St Louis, MO, Mosby Co, 1953.
17. Fitzgerald FT, Hypoglycemia and accidental hypothermia in an alcoholic population. West J Med 1980
18. Stoner HB et al., Metabolic aspects of hypothermia in the elderly. Clin Sci 1980
19. MacGregor DC et al., The effects of ether, ethanol, propanol and butanol on tolerance to deep hypothermia. Dis Chest 1966
20. Cooper KE, Hunter AR, and Keatinge WR, Accidental hypothermia. Int Anesthesia Clin 1964
21. Keatinge WR. The effects of subcutaneous fat and of previous exposure to cold on the body temperature, peripheral blood flow and metabolic rate of men in cold water. J Physiol 1960
22. Sloan REG and Keatinge WR, Cooling rates of young people swimming in cold water. J Appl Physiol 1973
23. Keatinge WR, Role of cold and immersion accidents. In Adam JM (Ed) Hypothermia – Ashore and Afloat. 1981, Chapter 4, Aberdeen Univ. Press, GB.
24. Keatinge WR and Evans M, The respiratory and cardiovascular responses to immersion in cold and warm water. QJ Exp Physiol 1961
25. Keatinge WR and Nadel JA, Immediate respiratory response to sudden cooling of the skin. J Appl Physiol 1965
26. Golden F. St C. and Hurvey GR, The “After Drop” and death after rescue from immersion in cold water. In Adam JM (Ed). Hypothermia – Ashore and Afloat, Chapter 5, Aberdeen Univ. Press, GB 1981.
27. Burton AC and Bazett HC, Study of average temperature of tissue, of exchange of heat and vasomotor responses in man by means of bath coloremeter. Am J Physiol 1936
28. Adam JM, Cold Weather: Its characteristics, dangers and assessment, In Adam JM (Ed).Hypothermia – Ashore and Afloat, Aberdeen Univ. Press, GB1981.
29. Modell JH and Davis JH, Electrolyte changes in human drowning victims.Anesthesiology 1969
30. Bolte RG, et al., The use of extracorporeal rewarming in a child submerged for 66 minutes. JAMA 1988
31. Ornato JP, The resuscitation of near-drowning victims. JAMA 1986
32. Conn AW and Barker CA: Fresh water drowning and near-drowning — An update.1984;
33. Reh H, On the early postmortem course of “washerwoman’s skin at the fingertips.” Z Rechtsmed 1984;
34. Gonzales TA, Vance M, Helpern M, Legal Medicine and Toxicology. New York, Appleton-Century Co, 1937.
35. Peabody AJ, Diatoms and drowning – A review, Med Sci Law 1980
36. Foged N, Diatoms and drowning — Once more.Forens Sci Int 1983
37. "Microscale chaotic advection enables robust convective DNA replication.". Analytical Chemistry. 2013
38. Sourcebook in Forensic Serology, Immunology, and Biochemistry (U.S. Department of Justice, National Institute of Justice, Washington, D.C.,1983).
39. C. A. Villee et al., Biology (Saunders College Publishing, Philadelphia, 2nd ed.,1989).
40. Molecular Biology of the Gene (Benjamin/Cummings Publishing Company, Menlo Park, CA, 4th ed., 1987).
41. Molecular Evolutionary Genetics (Plenum Press, New York,1985).
42. Human Physiology. An Integrate. 2016
43. Dumas JL and Walker N, Bilateral scapular fractures secondary to electrical shock. Arch. Orthopaed & Trauma Surg, 1992; 111(5)
44. Stueland DT, et al., Bilateral humeral fractures from electrically induced muscular spasm. J. of Emerg. Med. 1989
45. Shaheen MA and Sabet NA, Bilateral simultaneous fracture of the femoral neck following electrical shock. Injury. 1984
46. Rajam KH, et al., Fracture of vertebral bodies caused by accidental electric shock. J. Indian Med Assoc. 1976
47. Wright RK, Broisz HG, and Shuman M, The investigation of electrical injuries and deaths. Presented at the meeting of the American Academy of Forensic Science, Reno, NV, February 2000.
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