Introduction
Evidence of the time elapsed since death, the postmortem interval, may come from three sources: (1) the body of the deceased; (2) the environment in the vicinity of the body; and (3) information on the deceased’s habits, movements, and day-to-day activities. All three sources of evidence (corporal, environmental and anamnestic) should be explored and assessed before offering an opinion on when death occurred. The longer the postmortem interval then the less accurate is the estimate of it based upon corporal changes. As a consequence, the longer the postmortem interval then the more likely it is that associated or environmental evidence will provide the most reliable estimates of the time elapsed.
No problem in forensic medicine has been investigated as thoroughly as the determination of the postmortem interval on the basis of postmortem changes to the body. Many physicochemical 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 progresses at its own rate which, unfortunately, is strongly influenced by
Figure 5 Mummification: trapped in a heating duct for 7 years.
Postmortem Entomology and Other Artifacts
The common bluebottle or blowfly lays its eggs when the skin temperature falls below 27°C. The eggs rapidly hatch into maggots, which have a voracious appetite and invade all parts of the body, including the cranium, thorax and abdomen. Beetles lay their eggs on older bodies. Bodies immersed in water are not immune to insect activity. Caddis flies, water beetles, etc., in common with all insects, will ‘nibble’ at exposed surfaces, producing areas of apparent abrasion.
Animals such as rats and mice attack exposed parts of bodies. Foxes will also eat carrion. Even domestic dogs and cats will turn to their owners once the contents of the biscuit bowl have been exhausted. Fungi attack the skin even in embalmed and/or refrigerated bodies. When wiped away, the underlying exposed areas of skin are often discolored and roughened; these changes may lead to the mistaken diagnosis of bruises or abrasions sustained during life. Occasionally, a clumsily handled body may be damaged while being lifted into the coffin or wheeled through the corridors of a mortuary, producing abrasions upon the skin, usually over bony prominences. These abrasions are readily distinguished from ante-mortem injury. They are light brown in colour and rapidly become hard, shiny and slightly depressed. There is no vital reaction around them, and they show no microscopic changes of injury.
No problem in forensic medicine has been investigated as thoroughly as the determination of the postmortem interval on the basis of postmortem changes to the body. Many physicochemical 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 progresses at its own rate which, unfortunately, is strongly influenced by largely unpredictable endogenous and environmental factors. Consequently, using the evolution of postmortem changes to estimate the postmortem interval is invariably difficult, and always of limited accuracy.
Body Cooling
Body cooling (algor mortis or ‘the chill of death’) is the most useful single indicator of the postmortem interval during the first 24 h after death. Some authorities would regard it as the only worthwhile corporal method. The use of this method is only possible in cool and temperate climates, because in tropical regions there may be a minimal fall in body temperature postmortem, and in some extreme climates, such as desert regions, the body temperature may even rise after death.
Since body heat production ceases soon after death but loss of heat continues, the body cools. After death, as during life, the human body loses heat by radiation, convection and evaporation. The fall in body temperature after death is mainly the result of radiation and convection. Evaporation may be a significant factor if the body or clothing is wet. 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.
Newton’s law of cooling states that the rate of cooling of an object is determined by the difference between the temperature of the object and the temperature of its environment. A plot of temperature against time gives an exponential curve. However, Newton’s law applies to small inorganic objects and does not accurately describe the cooling of a corpse which has a large mass, an irregular shape, and is composed of tissues of different physical properties. The cooling of a human body is best represented by a sigmoid curve when temperature is plotted against time. Thus, 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 postmortem temperature plateau is physically determined and is not a special feature of the dead human body. Any inert body with a low thermal conductivity has such a plateau during its first cooling phase. The postmortem temperature plateau generally lasts between 30min and lh, but may persist for as long as 3 h, and some authorities claim that it may persist for as long as 5 h.
It is usually assumed that the body temperature at the time of death was normal. However, in individual cases the body temperature at death may be subnormal or markedly raised. As well as in deaths from hypothermia, the body temperature at death may be subnormal in cases of congestive cardiac failure, massive hemorrhage, and shock. The body temperature may be raised at the time of death following an intense struggle, in heat stroke, in some infections and in cases of pontine hemorrhage. The English forensic pathologist Simpson recorded a personal observation of a case of pontine hemorrhage with a temperature at death of 42.8°C (109°F). Where there is a fulminating infection, e.g. septicemia, 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 postmortem temperature plateau. For this reason assessment of time of death from body temperature cannot be accurate in the first 4-5 h 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, over the linear part of the sigmoid cooling curve, any formula which involves an averaging of the temperature decline per hour may well give a reasonably reliable approximation of the time elapsed since death. It is in this limited way that the cadaveric temperature may assist in estimating the time of death in the early postmortem period.
Unfortunately the linear rate of postmortem cooling is affected by environmental factors other than the environmental temperature and by cadaveric factors other than the body temperature at the time of death. The most important of these factors are body size, body clothing or coverings, air movement and humidity, and wetting or immersion in water.
Body size is a factor because 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. Children lose heat more quickly because their surface area to mass ratio is much greater than that of adults. 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 fetal position the proportion is only 60%.
Clothing and coverings insulate the body from the environment and therefore slow body cooling. The effect of clothing has a greater impact on corpses of low body weight. A bedspread covering may at least halve the rate of cooling. For practical purposes, only the clothing or covering of the lower trunk is relevant.
Air movement accelerates cooling by promoting convection, and even the slightest sustained air movement is significant if the body is naked, thinly clothed or wet. Cooling is more rapid in a humid rather than a dry atmosphere because moist air is a better conductor of heat. In addition, the humidity of the atmosphere will affect cooling by evaporation where the body or its clothing is wet. 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.
Simple formulae for estimating the time of death from body temperature are now regarded as naive. The literature is replete with formulae enthusiastically recommended at first and later disavowed. The best tested and most sophisticated current method for estimating the postmortem interval from body temperature is that of the German researcher Henssge. Even so, it is acknowledged that the method may produce occasional anomalous results. It uses a nomogram based upon a complex formula, which approximates the sigmoid-shaped cooling curve. To make the estimate of postmortem interval, using this method requires (1) the body weight, (2) the measured environmental temperature and (3) the measured deep rectal temperature, and assumes a normal body temperature at death of 37.2°C. Empiric corrective factors allow for the effect of important variables such as clothing, wetting and air movement. The use of these corrective factors requires an element of personal experience. At its most accurate, this sophisticated methodology provides an estimate of the time of death within a time span of 5.6 h with 95% probability. One of the most useful aspects of the nomogram is the ease with which the effect of changes in the variables can be tested. As a result it is an educational as well as a practical investigative tool.
The assessment of body cooling is made on the basis of measurement of the body core temperature, and, postmortem, this requires a direct measurement of the intraabdominal temperature. In practice either the temperature is measured rectally, or the intrahepa-tic/subhepatic temperature is measured through an abdominal wall stab. Oral, aural and axillary temperatures cannot be used because after death these are not reflective of the body core temperature. For the measurement, an ordinary clinical thermometer is useless because its temperature range is too narrow, and the thermometer is too short for insertion deep into the rectum or liver. A chemical thermometer 2530 cm (10-12 inches) long with a range from 0 to 50°C is ideal. Alternatively a thermocouple probe can be used, and this has the advantage of a digital readout or a programmable printed record.
Whether the temperature is measured via an abdominal stab or rectally is a matter of professional judgment 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 rectally. It may be necessary to make small slits in the clothing to gain access to the rectum, if the body is clothed and the garments cannot be pushed to one side. The chemical thermometer must be inserted about 7.5-10 cm (3-4 inches) into the rectum and read in situ. The alternative is to make an abdominal stab wound after displacing or slitting any overlying clothing. The stab can be made over the right lower ribs and the thermometer pushed into the substance of the liver, or alternatively a subcostal stab will allow insertion of the thermometer on to the undersurface of the liver. If a method of sequential measurements of body temperature is to be used, the thermometer should be left in situ during this period. Taking sequential readings is much easier with a thermocouple and an attached printout device.
The core body temperature should be recorded as early as conveniently possible at the scene of death. The prevailing 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. Temperature readings of the body represent data, which, if not collected, are irretrievably lost. Therefore the decision not to take such readings should always be a considered one.
Rigor Mortis
Ordinarily, death is followed immediately by total muscular relaxation, primary muscular flaccidity, succeeded in turn by generalized muscular stiffening, rigor mortis. After a variable period of time, as a result of the development of putrefaction, rigor mortis passes off spontaneously, to be followed by secondary muscular flaccidity. There is great variation in the rate of onset and the duration of rigor mortis, so that using the state of rigor mortis to estimate the postmortem interval is of very little value. In general, if the body has cooled to the environmental temperature and rigor is well developed, then death occurred more than 1 day previously and less than the time anticipated for the onset of putrefaction (see below), which is about 3-4 days in a temperate climate.
As a general rule, when the onset of rigor is rapid its duration is relatively short. The two main factors that influence the onset and duration of rigor are the environmental temperature and the degree of muscular activity before death. Onset of rigor is accelerated and its duration shortened when the environmental temperature is high, so that putrefaction may completely displace rigor within 9-12 h of death. If the temperature is below 10°C it is exceptional for rigor mortis to develop, but if the environmental temperature is then raised, rigor mortis will 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 can be explained by the lack of muscular activity immediately prior to death.
Classically, rigor is said to develop sequentially, but this is by no means constant, symmetrical or regular. Antemortem exertion usually causes rigor to develop first in the muscles used in the activity. Otherwise, rigor is typically first apparent in the small muscles of the eyelids, lower jaw and neck, followed by the limbs. It involves first the small distal joints of the hands and feet and then the larger proximal joints of the elbows, knees and then the shoulders and hips. It is generally accepted that rigor mortis passes off in the same order in which it develops. The forcible bending of a joint against the fixation of rigor results in tearing of the muscles and the rigor is said to have been ‘broken’. Provided the rigor had been fully established, it will not reappear once broken down by force. Re-establishment of rigor, albeit of lesser degree, after breaking it suggests that death occurred less than about 8 h before rigor was broken.
The intensity of rigor mortis depends upon the decedent’s muscular development, and should not be confused with its degree of development. In examining a body, both the degree (complete, partial or absent joint fixation) and the distribution of rigor should be assessed, after establishing that no artifact has been introduced by previous manipulation of the body by other observers. Attempted flexion of the different joints will indicate the degree and location of rigor. Typically slight rigor can be detected within a minimum of 30 min after death but may be delayed for up to 7 h. The average time of first appearance is 3h. It reaches a maximum, i.e. complete development, after an average 8 h, but sometimes as early as 2 h postmortem or as late as 20 h.
Livor Mortis
Lividity is a dark purple discoloration of the skin resulting from the gravitational pooling of blood in the veins and capillary beds of the dependent parts of the corpse. Synonyms include livor mortis, hypostasis, postmortem lividity, and, in the older literature, postmortem suggillations. Lividity is present in all corpses, although it may be inconspicuous in some. The med-icolegal importance of lividity lies in its color, as an indicator of cause of death, and in its distribution, as an indicator of body position. The development of livor is too variable to serve as a useful indicator ofthe postmortem interval, but the tradition of evaluating it remains entrenched in forensic practice.
Most authorities agree that lividity attains its maximum intensity, on average, at around 12 h postmortem, but there is some variation in descriptions of when it first appears, and when it is well developed, i.e. confluent. Hypostasis begins to form immediately after death, but it may not be visible for some time. Ordinarily its earliest appearance, as dull red patches, is 20-30 min after death, but this may be delayed for up to 2, or rarely 3 h. The patches of livor then deepen, increase in intensity, and become confluent within 14 h postmortem, to reach a maximum extent and intensity within about 6-10 h, but sometimes as early as 3 h or as late as 16 h. Faint lividity may appear shortly before death in individuals with terminal circulatory failure. Conversely, the development of lividity may be delayed in persons with chronic anemia or massive terminal hemorrhage.
After about 10-12 h the lividity becomes ‘fixed’ and repositioning the body, e.g. from the prone to the supine position, will result in a dual pattern of livid-ity, as the primary distribution will not fade completely but a secondary distribution will develop in the newly dependent parts. The blanching of livor by thumb pressure is a simple indicator that it is not fixed. Fixation of lividity is a relative, not an absolute, phenomenon. Well-developed lividity fades very slowly and only incompletely. Fading of the primary pattern and development of a secondary pattern of lividity will be quicker and more complete if the body is moved early during the first day. However, even after a postmortem interval of 24 h, moving the body may result in a secondary pattern of lividity developing. Duality of the distibution of lividity is important because it shows that the body has been moved after death. However, it is not possible to estimate with any precision, from the dual pattern of livor, when it was that the corpse was moved.
Areas of lividity are overtaken early in the putrefactive process. The red cells are hemolyzed and the hemoglobin diffuses into the surrounding tissues, where it may undergo secondary changes such as sulfhemoglobin formation.
Putrefaction
Putrefaction is the postmortem destruction of the soft tissues of the body by the action of bacteria and endogenous enzymes. The main changes recognizable in the tissues undergoing putrefaction are changes in color, the evolution of gases, and liquefaction. The green discoloration seen is due to sulfhemoglobin formation. The gases produced include hydrogen sulfide, methane, carbon dioxide, ammonia and hydrogen. The offensive odor is caused by some of these gases and by small quantities of mercaptans.
Bacteria are essential to putrefaction, and commensal bacteria soon invade the tissues after death. Typically, the first visible sign of putrefaction is a greenish discoloration of the skin of the anterior abdominal wall. This most commonly begins in the right iliac fossa, i.e. over the area of the cecum, where the contents of the bowel are more fluid and full of bacteria. Any antemortem bacterial infection of the body, particularly septicemia, will hasten the onset and evolution of putrefaction. Injuries to the body surface promote putrefaction by providing portals of entry for bacteria. Putrefaction is delayed in deaths from exsanguination because blood usually provides a channel for the spread of putrefactive organisms within the body. Although it tends to be more rapid in children than in adults, the onset is relatively slow in unfed newborn infants because of the lack of commensal bacteria in the gut.
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 a temperate climate, the degree of putrefaction reached after 24 h in the height of summer may require 10-14 days in the depth of winter. Putrefaction is optimal at temperatures ranging between 21 and 38° C (70 and 100°F), and is retarded when the temperature falls below 10°C (50°F) or when it exceeds 38°C (100°F).
A high environmental humidity will enhance putrefaction. Heavy clothing and other coverings, by retaining body heat, will speed up putrefaction. The rate of putrefaction is influenced by body build because this affects body cooling (see above). Obese individuals putrefy more rapidly than those who are lean. 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.
There is considerable variation in the time of onset and the rate of progression of putrefaction. As a result, the time taken to reach a given state of putrefaction cannot be judged with accuracy. An observer should not assert too readily that the decomposed state of a body is inconsistent with a time interval alleged. As a general rule, when the onset of putrefaction is rapid then the progress is accelerated. Under average conditions in a temperate climate the earliest putrefactive changes involving the anterior abdominal wall occur between 36 and 72 h after death. Progression to gas formation, and bloating of the body, occurs after about 1 week. The temperature of the body after death is the most important factor generally determining the rate of putrefaction. If it is maintained above 26°C (80°F) then the putrefactive changes become obvious within 24 h and gas formation is seen in about 2-3 days.
According to an old rule of thumb (Casper’s dictum), 1 week of putrefaction in air is equivalent to 2 weeks in water, which is equivalent to 8 weeks buried in soil, given the same environmental temperature. After normal burial, the rate at which the body decomposes will depend to a large extent on the depth of the grave, the warmth of the soil, the efficiency of the drainage and the permeability of the coffin. The putrefactive changes are relatively rapid when contrasted with the terminal decay of the body. When the putrefactive juices have drained away and the soft tissues have shrunk, the speed of decay is appreciably reduced.
Adipocere
Saponification or adipocere formation is a modification of putrefaction characterized by the transformation of fatty tissues into a yellowish-white, greasy (but friable when dry), wax-like substance, which has a sweetish rancid odor when its formation is complete. During the early stages of its production a penetrating and very persistent ammoniacal smell is emitted. Adipocere develops as the result of hydrolysis of fat with the release of fatty acids, which, being acidic, then inhibit putrefactive bacteria. However, fat and water alone do not produce adipocere. Putrefactive organisms, of which Clostridium welchii is the most active, are important, and adipocere formation is facilitated by postmortem invasion of the tissues by commensal bacteria. A warm, moist, anaerobic environment thus favors adipocere formation.
Adipocere develops first in the subcutaneous tissues, most commonly involving the cheeks, breasts and buttocks. Rarely, it may involve the viscera, such as the liver. The adipocere is admixed with the mummified remains of muscles, fibrous tissues and nerves. The primary medicolegal importance of adipocere lies not in establishing the postmortem interval but rather in the preservation of the body, which aids in personal identification and the recognition of injuries.
The presence of any adipocere indicates that the postmortem interval is at least weeks and probably several months. Under ideal warm, damp conditions, adipocere may be apparent to the naked eye after 3-4 weeks. Ordinarily, this requires some months and extensive adipocere is usually not seen before 5 or 6 months after death. Some authorities suggest that extensive changes require not less than a year after submersion, or upwards of 3 years after burial. Once formed, adipocere will ordinarily remain unchanged for years.
Mummification
Mummification is a modification of putrefaction characterized 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. Mummification develops in conditions of dry heat, especially when there are air currents, e.g. in a desert. Newborn infants, being small and sterile, commonly mummify. Mummification of bodies of adults in temperate climates is unusual unless associated with forced hot-air heating in buildings or other manmade favorable 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 fetus, which has died in the uterus and remained enclosed within the amniotic sac. Bacterial putrefaction plays no role in the process. The changes of maceration are only seen when a stillborn fetus has been dead for several days before delivery. Examination of the body needs to be prompt because bacterial putrefaction will begin following delivery. The body is extremely flaccid, with a flattened head and undue mobility of the skull. The limbs may be readily separated from the body. There are large, moist skin bullae, which rupture to disclose a reddish-brown surface denuded of epidermis. Skin slip discloses similar underlying discoloration. The body has a rancid odor but there is no gas formation. Establishing maceration of the fetus provides proof of a postmortem interval in the uterus, and therefore proof of stillbirth and conclusive evidence against infanticide.
Vitreous Potassium
Several researchers have studied the relationship between the potassium concentration of the vitreous humor of the eye and the postmortem interval. However, within 100 h postmortem, the 95% confidence limits of the different researchers vary from + 9.5 h up to + 40 h. Cases with possible confounding ante-mortem electrolyte disturbances can be excluded by eliminating all cases with a vitreous urea above an arbitrary level of 100mgdl_1. (High urea values in vitreous humor always reflect antemortem retention and are not due to postmortem changes.) Having eliminated these cases, there is a linear relationship between vitreous potassium concentration and time elapsed after death up to 120 h. However, the 95% confidence limits are + 22 h, so that the method has no real practical application. There are also sampling problems, in that the potassium concentration may differ significantly between the left and right eye at the same moment.
