Medico-legal Problems of establishing the Time of Death

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. Determining the time of death is of utmost importance but it is extremely difficult and accuracy is impossible. A recurring problem in forensic medicine is the need to fix the time of death within the limits of probability, 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.

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 illness 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.

Three Sources of Evidence for estimating the time of death:

Corporal evidence; that present in the body.
Environmental and associated evidence; that present in the vicinity of the body.
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.

Two methods for estimating the time of death:

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.

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.

Various postmortem changes which may give the forensic scientist an approximate evaluation of the possible 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 and therefore, 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. Some writers would regard it as the only worthwhile corporal method. It is of some importance to note that the use of body temperature estimations to assess time of death applies only to cool and temperate climates since in tropical regions there may be a minimal fall in body temperature post mortem and in some extreme climates, (e.g. central Australia) the body temperature may rise even after death.

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. The normal oral temperature fluctuates between 35.9C and 37.2C. In practice either the temperature is measured per rectum or via an abdominal stab. Oral temperatures should not be used but a chemical thermometer long with a range from 0-50C is ideal. Alternatively a thermo-couple probe may be used and this has the advantage of a digital readout or a printed record. Whether the temperature is measured via an abdominal stab or per rectum is a matter of professional judgement in each case. If there is easy access to the rectum without the need to seriously disturb the position of the body and if there is no reason to suspect sexual assault, then the temperature can be measured per rectum. The alternative is to make an abdominal stab wound after displacing or slitting any overlying clothing. The stab may be over the lower ribs and the thermometer inserted within the substance of the liver or alternatively a subcostal stab will allow insertion of the thermometer onto the undersurface of the liver.

The body temperature should be recorded as early as conveniently possible. The environmental temperature should also be recorded and a note made of the environmental conditions at the time the body was first discovered and any subsequent variation in these conditions. If a method of sequential measurement of body temperature is use then the thermometer should be left in situ during this time period. 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.

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.

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There is an initial maintenance of body temperature which may last for some hours - the so-called "temperature plateau" - followed by a relatively linear rate of cooling which subsequently slows rapidly as the body approaches the environmental temperature. The post mortem temperature plateau generally lasts half to one hour but may persist as long as three hours and some authorities claim that it may persist as long as five hours. It is usually assumed that the body temperature at the time of death is normal, but in individual cases it may be subnormal or markedly raised. As well as in deaths from hypothermia, the body temperature at death may be sub-normal in cases of cardiac failure, massive haemorrhage, and shock. However, the claim that severe agonal bleeding lowers the body temperature is said to be without foundation. The body temperature may be raised at the time of death in heat stroke, some infections, and pontine haemorrhage. Simpson cites a personal observation of a case of pontine haemorrhage with an initial temperature at death of 42.8C and another instance of a temperature of 37.4C about three hours after death in a case of manual strangulation. However, another author claims that there is no convincing proof that asphyxia by strangulation leads to a raised agonal temperature. Where there is a serious infection like septicaemia, the body temperature may continue to rise for some hours after death.

Thus the two important unknowns in assessing time of death from body temperature are (1) the actual body temperature at the time of death; and (2) the actual length of the post mortem temperature plateau. For this reason assessment of time of death from body temperature clearly cannot be accurate, (even approximately), in the first four to five hours after death when these two unknown factors have a dominant influence. Similarly, body temperature cannot be a useful guide to time of death when the cadaveric temperature approaches that of the environment. However, in the intervening period any formula which involves an averaging of the temperature decline per hour may well give a reasonably reliable approximation of the time of death. It is in this limited way that the cadaveric temperature may assist in estimating the time of death in the early post mortem interval, provided the sigmoid nature of the relationship between the temperature of the cooling body and that of its environment is kept in mind. The linear rate of post mortem cooling is affected by environmental factors and cadaveric factors other than the environmental temperature and the body temperature at the time of death. These include:

1. The "size" of the body; the greater the surface area of the body relative to its mass, the more rapid will be its cooling. Consequently, the heavier the physique and the greater the obesity of the body, the slower will be the heat loss. Some authors claim that in obese individuals the fat acts as an insulator, but for practical purposes body mass is the most important factor. Children lose heat more quickly than adults because their surface area/mass ratio is much greater. Prominent oedema in individuals with congestive cardiac failure is said to retard cooling because of the large volume of water present with a high specific heat whilst dehydration has the opposite effect. The effect of oedema fluid is said to be more potent than body fat. The exposed surface area of the body radiating heat to the environment will vary with the body position. If the body is supine and extended, only 80% of the total surface area effectively loses heat, and in the foetal position the proportion is only 60%.

2. Clothing and coverings; these insulate the body from the environment and therefore cooling is slower. Simpson states that cooling of a naked body is half again as fast as when clothed. Henssge has graded the effect of clothing by the number of layers and thickness. He states that only the clothing or covering of the lower trunk is relevant.

3. Movement and air humidity; Air movement accelerates cooling by promoting convection and even the slightest sustained air movement is significant. Cooling is said to be more rapid in a humid rather than dry atmosphere because moist air is a better conductor of heat. The humidity of the atmosphere will affect cooling by evaporation where the body or its clothing is wet.

4. Immersion in water; A cadaver cools more rapidly in water than in air because water is a far better conductor of heat. For a given environmental temperature, cooling in still water is about twice as fast as in air, and in flowing water, about three times as fast. Clearly the body will cool more rapidly in cold water than warm water. It has been claimed that bodies will cool more slowly in water containing sewage effluent or other putrefying organic matter than in fresh water or sea water. The author does not state whether this factor is claimed to be independent of water temperature.

Simple formulae for estimating the time of death are now regarded as naive. These include the formula of Simpson - "under average conditions the clothed body will cool in air at the rate of about 1.5C an hour for the first 6 hours and average a loss of some 1C for the first 12". The best researched and documented method for assessing time of death from body temperature is that of Henssge. This is a nomogram method rather than a formula. The nomogram corrects for any given environmental temperature. It requires the measurement of deep rectal temperature and assumes a normal temperature at death of 37.2C.

It is well recognised that the presence of layers of clothing, wetting of the clothing, and air movement, all influence the rate of body cooling. Similarly, bodies in still and flowing water cool more rapidly than in air.

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. 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. 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.

Rigor mortis results from a physico-chemical change in muscle protein, the precise nature of which is unknown. Classically, rigor is said to develop sequentially, but this is by no means constant, symmetrical or regular. Ante-mortem exertion usually causes rigor to develop first in the muscles used in the activity. Typically, rigor is first apparent in the small muscles of the eyelids, lower jaw and neck, followed by the limbs, involving first the small distal joints of the hands and feet and then the larger proximal joints of the elbows, knees and the shoulders and hips. In temperate climates rigor will typically start to disappear at about 36-48 hours after death. However, if the environmental temperature is high then the development of putrefaction may completely displace rigor within 9-12 hours of death. Accelerated putrefaction resulting from ante-mortem septicaemia may also lead to a rapid displacement of rigor.

As a general rule when the onset of rigor is rapid, then its duration is relatively short. The two main factors which influence the onset and duration of rigor are (a) the environmental temperature, and (b) the degree of muscular activity before death. Onset of rigor is accelerated and its duration shortened when the environmental temperature is high. If the temperature is below 10C it is said to be exceptional for rigor mortis to develop, but if the environmental temperature is then raised, rigor mortis is said to develop in a normal manner. Rigor mortis is rapid in onset and of short duration after prolonged muscular activity, e.g. after exhaustion in battle, and following convulsions. Conversely, a late onset of rigor in many sudden deaths might be explained by the lack of muscular activity immediately prior to death.

Other endogenous and environmental factors are claimed to influence the onset of rigor. It develops early and passes quickly in deaths from septicaemia or from wasting diseases. It is delayed in asphyxial deaths, notably by hanging or carbon monoxide poisoning, and also when death has been immediately preceded by severe haemorrhage.

Knight states that "it is extremely unsafe to use rigor at all in the estimation of time since death" is somewhat extreme. However, Camps’ thoery is overly simplistic - "corpses can usually be divided into those, still warm, in which no rigor is present, indicating death within about the previous three hours. Those in which rigor is progressing, where death probably occurred between 2 and 9 hours previously; and those in which rigor is fully established, showing that death took place more than 9 hours previously". If full rigor is present, then one might assume that this is about the second day following death, depending upon the environmental conditions.

Exposure of a body to intense heat results in heat stiffening due to coagulation of the muscle proteins. Unlike rigor mortis, heat stiffening is associated with muscle shortening resulting in the characteristic pugilistic posture of burned bodies. Heat stiffening obscures rigor mortis with which it should not be confused. Freezing of a body will cause stiffening of the muscles, postponing the development of rigor which is said to develop as soon as thawing of the body permits.

Cadaveric Spasm (instantaneous rigor, instantaneous rigidity) is a form of muscular stiffening which occurs at the moment of death and which persists into the period of rigor mortis. Its cause is unknown but it is usually associated with violent deaths in circumstances of intense emotion. It has medico-legal importance because it records the last act of life. Cadaveric spasm may affect all the muscles of the body but it most commonly involves groups of muscles only, such as the muscles of the forearms and hands. Should an object be held in the hand, then cadaveric spasm should only be diagnosed if the object is firmly held and considerable force is required to break the grip. Cadaveric spasm is seen in a small proportion of suicidal deaths from firearms, incised wounds, and stab wounds, when the weapon is firmly grasped in the hand at the moment of death. In such circumstances the gripping of the weapon creates a presumption of self-infliction of the injuries. This state cannot be reproduced after death by placing a weapon in the hands. It is also seen in cases of drowning when grass, weeds, or other materials are clutched by the deceased. In this circumstance, it provides proof of life at the time of entry into the water. Similarly, in mountain fatalities, branches of shrubs or trees may be seized. In some homicides, hair or clothing of the assailant may be found in the hands of the deceased.

LIVOR MORTIS (HYPOSTASIS, POST MORTEM LIVIDITY)

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. The medico-legal importance of post mortem lividity lies in its colour and in its distribution. The development of lividity is too variable to serve as a useful indicator of the time of death.

Lividity is first apparent about 20-30 minutes after death as dull red patches or blotches which deepen in intensity and coalesce over the succeeding hours to form extensive areas of reddish-purple discolouration. Slight lividity may appear shortly before death in individuals with terminal circulatory failure. After about 10-12 hours the lividity becomes "fixed" and repositioning the body, e.g. from the prone to the supine position, will result in a dual pattern of lividity since the primary distribution will not fade completely. Even after 24 hours, moving the body will result in a secondary pattern of lividity developing. Duality of the distribution of lividity is important because it shows that the body had been moved after death. However, the timing of this movement of the body is inexact. A supine corpse will display contact pallor over the shoulderblades, buttocks, calves and heels. Other areas of contact pallor will correspond with the location of firm fitting clothing, e.g. elasticated underwear, belts and collars, and any firm object lying beneath the body, e.g. the arm of the decedent. Thus, the distribution of lividity depends upon the position of the body after death. In a decomposing body it may be impossible to definitively distinguish between livid staining of the tissues and a putrefying area of bruising. Areas of lividity are overtaken early in the putrefactive process.

Most texts agree that lividity attains its maximum intensity at around 12 hours post mortem, but there is some variation in descriptions of when it first appears, and when it is well developed. Simpson states that "it commences to develop within an hour or so of death, becoming marked in 5 or 6 hours".

POSTMORTEM DECOMPOSITION (PUTREFACTION)

Putrefaction is the post mortem destruction of the soft tissues of the body by the action of bacteria and enzymes. Tissue breakdown resulting from the action of endogenous enzymes alone, 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. Bacteria are essential to putrefaction and commensal bacteria soon invade the tissues after death. Any ante-mortem bacterial infection of the body, particularly scepticaemia, will hasten the onset and evolution of putrefaction. Environmental temperature has a very great influence on the rate of development of putrefaction so that rapid cooling of the body following a sudden death will markedly delay its onset. In the temperate climate of England the degree of putrefaction reached after twenty-four hours in the height of summer may require ten to fourteen days in the depth of winter. A high environmental humidity will enhance putrefaction. Putrefaction is optimal at temperatures ranging between 21-38C and is retarded when the temperature falls below 10C or when it exceeds 38C.

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. Putrefaction is accelerated when the tissues are oedematous, e.g. in deaths from congestive cardiac failure, and delayed when the tissues are dehydrated. 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 be seen in corpses left in a well heated room 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.

Under average conditions in a temperate climate the earliest putrefactive changes involving the anterior abdominal wall occur between thirty-six and seventy-two hours after death. Progression to gas formation occurs after about one week. The temperature of the body after death is the most important factor generally determining the rate of putrefaction. If it is maintained above 26C after death then putrefactive changes become obvious within 24 hours and gas formation will be seen in about 2-3 days.

ADIPOCERE

Saponification or adipocere formation is a modification of putrefaction characterised by the transformation of fatty tissues into a yellowish-white, greasy, wax-like substance, with a sweetish rancid odour. 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, but ordinarily it will remain unchanged for years.

Adipocere develops as the result of hydrolysis of fat with the release of fatty acids which then inhibit putrefactive bacteria. A warm, moist, anaerobic environment favours adipocere formation. It was once thought that adipocere required immersion in water or damp conditions for its development. However, the water content of a body may be sufficient in itself to induce adipocere formation in corpses buried in well sealed coffins.

The final product is of a larger bulk than the original fat with the result that external wounds may become closed and the pattern of clothing or ligatures may be imprinted on the body surface. Under ideal warm, damp conditions, adipocere may be apparent to the naked eye after 3-4 weeks. Ordinarily, adipocere formation requires some months and extensive adipocere is usually not seen before 5 or 6 months after death. Other authors suggest that extensive changes require not less than a year after submersion, or upwards of three years after burial.

The medico-legal importance of adipocere lies not in establishing time of death but rather in its ability to preserve the body to an extent which can aid in personal identification and the recognition of injuries. The presence of adipocere indicates that the post mortem interval is at least weeks and probably several months.

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.

Mummification develops in conditions of dry heat, especially when there are air currents, e.g. in a desert or inside a chimney. 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.

VITREOUS HUMOUR POTASSIUM

The relationship between the rise of potassium concentration in the vitreous humour and the time since death has been studied by several forensic scientists. An obstacle to using potassium concentration in vitreous humour as an aid in estimating the time since death are the different confidence limits given by different authors. There are also sampling problems in that the potassium concentration may differ significantly between the left and right eye at the same moment in time. Simultaneous sampling of both eyes has shown that the potassium concentration in one eye can deviate by up to 10% from the mean value of both eyes.

In conclusion, establishing the times of an assault and death has a direct bearing on the legal questions of alibi and opportunity. If the suspect is able to prove that he was at some other place when the fatal injury was inflicted then he has an alibi and his innocence is implicit. Conversely, if the time of a lethal assault coincides with the time when the suspect was known to be in the vicinity of the victim, then the suspect clearly had an opportunity to commit the crime. In cases of infanticide, it is necessary for the prosecution to establish that the child was born alive and was killed afterwards. In the absence of proof that death occurred after a live birth, there can be no prosecution for infanticide. Similarly, in bodies recovered from fires, it is critical to establish whether death occurred before or during the fire and this necessitates correlating information relevant to establishing both the time of death and the cause of death. When a body is recovered from water, a critical question is whether the person was alive or dead when they entered the water. Determining whether specific injuries were inflicted before or after death is another important example of establishing temporal relationships.

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