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POSTMORTEM CHANGES AND TIME OF DEATH

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ABSTRACT
No problem in forensic medicine has been investigated as thoroughly as that of determining the time of death on the basis of post mortem findings. Apart from its obvious legal importance, its solution has been so elusive as to provide a constant intellectual challenge to workers in many sciences. In spite of the great effort and ingenuity expended, the results have been meagre.

KeyWords : post mortem , time of death, algor mortis

Introduction

"The time of death is sometimes extremely important. It is a question almost invariably asked by police officers, sometimes with a touching faith in the accuracy of the estimate. Determining the time of death is extremely difficult, and accuracy is impossible". It is necessary to be alert to the possibility that the post mortem interval (the time elapsed from death until discovery and medical examination of the body) may be preceded by a significant survival period (the time from injury or onset of the terminal illess to death). The survival interval is best established by evaluating the types, severity and number of injuries present and the deceased's response to them, taking into account pre-existing natural disease. At autopsy it is necessary to assess the evolution of the inflammatory response and repair process in skin and viscera.

Sources of Evidence

Evidence for estimating the time of death may come from three sources:
1.Corporal evidence, i.e. that present in the body.
2. Environmental and associated evidence, i.e. that present in the vicinity of the body,
3. Anamnestic evidence, i.e. that based on the deceased's ordinary habits, movements, and day to day activities.
All three sources of evidence should be explored and assessed before offering an opinion on when death or a fatal injury occurred.

There are two methods for estimating the time of death:

1. The rate method. Measuring the change produced by a process which takes place at a known rate which was either initiated or stopped by the event under investigation, i.e. death. Examples include the amount and distribution of rigor mortis, the change in body temperature, and the degree of putrefaction of the body.

2. The concurrence method. Comparing the occurrence of events which took place at known times with the time of occurrence of the event under investigation, i.e. death. For example, a wrist watch stopped by a blow during an assault, the extent of digestion of the last known meal.

Postmortem changes and time of death

Many physico-chemical changes begin to take place in the body immediately or shortly after death and progress in a fairly orderly fashion until the body disintegrates. Each change has its own time factor or rate. Unfortunately, these rates of development of post mortem changes are strongly influenced by unpredictable endogenous and environmental factors. Consequently, the longer the post mortem interval, the wider is the range of estimate as to when death probably occurred. In other words, the longer the post mortem interval, the less precise is the estimate of the time of death.

ALGOR MORTIS (BODY COOLING)
This is the most useful single indicator of the time of death during the first 24 hours post mortem.The assessment is made on the basis of measurement of the body core temperature which, post mortem, requires a direct measurement of the intra-abdominal temperature.

In practice either the temperature is measured per rectum or the intra-hepatic/sub-hepatic temperature is measured via an abdominal stab. Oral and axillary temperatures should not be used. An ordinary clinical thermometer is useless because its range is too small and the thermometer is too short. A chemical thermometer 10-12 long with a range from 0-50 Celsius is ideal. Alternatively a thermo-couple probe may be used and this has the advantage of a digital readout or a printed record. Temperature readings of the body and observations made at the scene by one physician are always available for evaluation by an expert at a later time. The normal oral temperature fluctuates between 35.9oC (96.7oF) and 37.2oC (99oF). The rectal temperature is from 0.3-0.4oC (0.5o-0.75oF) higher (cited in reference 19 at p. 12). Since heat production ceases soon after death but loss of heat continues, the body cools.

During life the human body loses heat by radiation, convection, and evaporation. Heat loss by conduction is not an important factor during life, but after death it may be considerable if the body is lying on a cold surface. The fall in body temperature after death mainly depends upon a loss of heat through radiation and convection, but evaporation may be a significant factor if the body or clothing is wet. The cooling of a body is a predominantly physical process which, therefore, is predominantly determined by physical rules.

RIGOR MORTIS
Ordinarily, death is followed immediately by total muscular relaxation - primary muscular flaccidity - succeeded in turn by generalised muscular stiffening - rigor mortis. After a variable period of time rigor mortis passes off spontaneously to be followed by secondary muscular flaccidity. The first investigation of rigor mortis is attributed to Nysten in 1811.

No measurable shortening of muscle occurs during rigor mortis unless the muscles are subjected to tension. When rigor is fully developed, the joints of the body become fixed, and the state of flexion or extension of these joints depends upon the position of the trunk and limbs at the time of death. If the body is supine then the large joints of the limbs become slightly flexed during the development of rigor. The joints of the fingers and toes are often markedly flexed due to the shortening of the muscles of the forearms and legs. Since significant muscle shortening is not a normal concomitant of rigor, it is unlikely that rigor mortis would cause any significant change in the attitude adopted by the corpse at death. The view that the development of rigor mortis could produce significant movements of the body was promoted by Sommer, in about 1833, and the postulated movements became known as "Sommer's movements". It is now accepted that movements of a corpse due to the development of rigor mortis can only occur in special circumstances, such as an extreme position of the body at the moment of death. If a body is moved before the onset of rigor then the joints will become fixed in the new position in which the body is placed. For this reason, when a body is found in a certain position with rigor mortis fully developed, it cannot be assumed that the deceased necessarily died in that position. Conversely, if the body is maintained by rigor in a position not obviously associated with support of the body, then it can be concluded that the body was moved after rigor mortis had developed.

LIVOR MORTIS
(HYPOSTASIS, POST MORTEM LIVIDITY, POSTMORTEM SUGGILLATIONS)
Lividity is a dark purple discolouration of the skin resulting from the gravitational pooling of blood in the veins and capillary beds of the dependent parts of the body following cessation of the circulation. The process begins immediately after the circulation stops, and in a person dying slowly with circulatory failure, it may be pronounced very shortly after death. Lividity is present in all bodies, although it may be inconspicuous in some and thus escape notice. Lividity is able to develop post mortem under the influence of gravity because the blood remains liquid rather than coagulating throughout the vascular system. Within about 30-60 minutes of death the blood in most corpses, dead from natural or non-natural causes, becomes permanently incoagulable. This is due to the release of fibrinolysins, especially from small calibre vessels, e.g. capillaries, and from serous surfaces, e.g. the pleura.
Clots may persist when the mass of clot is too large to be liquified by the fibrinolysin available at the site of clot formation. In some deaths associated with infection and cachexia, this fibrinolytic effect may fail to develop, explaining the presence of abundant clot in the heart and large calibre vessels. Thus, in cases of sudden death the blood remains spontaneously coagulable only during a brief period immediately following death; it then becomes completely free from fibrinogen and will never again clot. This incoagulability of the blood is a commonplace observation at autopsy. The fluidity of the blood is not characteristic of any special cause or mechanism of death although many texts state that the blood remains liquid longer in asphyxial deaths.

POSTMORTEM DECOMPOSITION - (PUTREFACTION )
Putrefaction is the post mortem destruction of the soft tissues of the body by the action of bacteria and enzymes (both bacterial and endogenous). Tissue breakdown resulting from the action of endogenous enzymes alone is known as autolysis. Putrefaction results in the gradual dissolution of the tissues into gases, liquids and salts. The main changes which can be recognised in the tissues undergoing putrefaction are changes in colour, the evolution of gases, and liquefaction. The rate of putrefaction is influenced by the bodily habitus of the decedent; obese individuals putrefy more rapidly than those who are lean. Putrefaction will be delayed in deaths from exsanguination because blood provides a channel for the spread of putrefactive organisms within the body. Conversely, putrefaction is more rapid in persons dying with widespread infection, congestive cardiac failure or anasarca.
Putrefaction is accelerated when the tissues are oedematous, e.g. in deaths from congestive cardiac failure, and delayed when the tissues are dehydrated. It tends to be more rapid in children than in adults, but the onset is relatively slow in unfed new-born infants because of the lack of commensal bacteria. Whereas warm temperatures enhance putrefaction, intense heat produces "heat fixation" of tissues and inactivates autolytic enzymes with a resultant delay in the onset and course of decomposition. Heavy clothing and other coverings, by retaining body heat, will speed up putrefaction. Rapid putrefactive changes may been seen in corpses left in a room which is well heated, or in a bed with an electric blanket. Injuries to the body surface promote putrefaction by providing portals of entry for bacteria and the associated blood provides an excellent medium for bacterial growth.

ADIPOCERE
Saponification or adipocere formation is a modification of putrefaction characterised by the transformation of fatty tissues into a yellowish-white, greasy, (but friable when dry), wax-like substance, with a sweetish rancid odour. Many states that when its formation is complete it has a sweetish smell, but during the early stages of its production a penetrating ammoniacal odour is emitted and the smell is very persistent. It floats on water, and dissolves in hot alcohol and ether. When heated it melts and then burns with a yellow flame. Ordinarily it will remain unchanged for years.

MUMMIFICATION
Mummification is a modification of putrefaction characterised by the dehydration or dessication of the tissues. The body shrivels and is converted into a leathery or parchment-like mass of skin and tendons surrounding the bone. The internal organs are often decomposed but may be preserved. Skin shrinkage may produce large artefactual splits mimmicking injuries. These are particularly seen in the groins, around the neck, and the armpits. Mummification develops in conditions of dry heat, especially when there are air currents, e.g. in a desert or inside a chimney. New-born infants, being small and sterile, commonly mummify. Mummification of bodies of adults in temperate climates is unusual unless associated with forced air heating in buildings or other man-made favourable conditions.
The forensic importance of mummification lies primarily in the preservation of tissues which aids in personal identification and the recognition of injuries. The time required for complete mummification of a body cannot be precisely stated, but in ideal conditions mummification may be well advanced by the end of a few weeks.

MACERATION
Maceration is the aseptic autolysis of a foetus which has died in utero and remained enclosed within the amniotic sac. Bacterial putrefaction plays no role in the process. The changes of maceration are only seen when a still-born foetus has been dead for several days before delivery. Normally the changes take about one week to develop.

Conclusion

A recurring problem in forensic medicine is the need to fix the time of death within the limits of probability. It is self-evident that the longer the interval of time between death and the examination of the body, the wider will be the limits of probability. The longer the post mortem interval, the more likely it is that associated or environmental evidence will furnish more reliable data on which to estimate the time of death than will anatomical changes.

References
1. Kerr, Forensic Medicine, 2nd edition, (1936), A. & C. Black, Ltd., London.
2. Rentoul and Smith, Glaister's Medical Jurisprudence and Toxicology, 13th edition, (1973), Churchill Livingstone, Edinburgh.
3. Watson, Forensic Medicine: A Handbook for Professionals (1989), Gower Press, Aldershot.
4. Mason, Forensic Medicine for Lawyers, 2nd edition, (1983), Butterworths, London.
5. Camps and Cameron, Practical Forensic Medicine (1971), Hutchinson Medical Publications, London.
6. Camps, Lucas, Robinson, Gradwohl's Legal Medicine, 3rd edition, (1976), John Wright & Sons, Bristol.
7. Gee and Watson, Lecture Notes on Forensic Medicine, 5th edition, (1989), Blackwell Scientific Publications, Oxford.
8. Knight, Legal Aspects of Medical Practice, 4th edition, (1987), Churchill Livingstone, Edinburgh.
9. Mant, Forensic Medicine (1960), Lloyd-Luke (Medical books) Ltd., London.
10. Polson, Gee and Knight, The Essentials of Forensic Medicine, 4th edition, (1985), Pergamon Press, Oxford.
11. Simpson and Knight, Forensic Medicine, 9th edition, (1988), Butler & Tanner Ltd., London.
12. Adelson, The Pathology of Homicide, (1974), Thomas, Springfield, Illinois.
13. Gonzales, Vance, Helpern, Umberger, Legal Medicine, Pathology and Toxicology, 2nd edition (1954), Appleton-Century Crofts, New York.
14. Spitz and Fisher, Medicolegal Investigation of Death, 2nd edition, (1980), Thomas, Springfield, Illinois.
15. Jaffe, A Guide to Pathological Evidence : For Lawyers and Police Officers, 2nd edition, (1983), Carswell Criminal Law Series, Carswell Ltd., Toronto.

Dr. Manjul Tiwari
MDS ,Oral Pathology & Microbiology
Senior Lecturer ,Hindustan Institute of Dental Sciences
Plot No. 32-34 , Knowledge Park – III
Greater Noida -201306
Uttar Pradesh


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