Time of Death
The methods cited here are somewhat unreliable and inaccurate, usually giving vague or dubious answers. The
longer the time between death and the attempt to determine the time of death, the less precise the estimate of the
interval. The time the fatal injury has incurred is not necessarily the time of death.
Factors that can be used in determining the time of death:
1. Livor mortis
Lividity or postmortem hypostasis is a reddish-purple coloration in determined areas of the body due to the
accumulation of blood in the small vessels secondary to gravity. It can be misinterpreted as bruising by people
unfamiliar with this phenomenon. Dependent areas resting against a hard surface will appear pale in contrast to
the surrounding livor mortis due to compression of the vessels in those areas (no accumulation of blood). Areas
supporting the weight of the body (shoulder blades, buttocks, and calves) in individuals lying on their backs,
appear as pale areas. Tight clothing can compress soft tissues, collapsing the vessels, also producing pale areas.
Livor mortis usually has a cherry-red to pinkish color in deaths due to carbon monoxide, caused by
carboxyhemoglobin. That can also happen by exposure of a body to cold temperatures, and in deaths by cyanide.
Localized areas of bright red livor mortis are also seen adjacent to chest tubes. In all three of the aforementioned
entities, the coloration is caused by the predominance of oxygenated hemoglobin.
It is usually evident within 30 min to 2h after death. In individuals dying slowly, with terminal cardiac failure,
livor mortis may appear antemortem. Livor mortis develops gradually, usually reaching its maximum coloration
at 8–12h, when it is said to become “fixed”; before it will shift as the body is moved. If an individual dies lying
on his back, it will develop posteriorly on the back. If one turns the body on its face, blood will drain to the
anterior surface of the body, now the dependent aspect. It becomes “fixed” when shifting or drainage of blood no
longer occurs, or when blood leaks out of the vessels into the surrounding soft tissue due to hemolysis and
breakdown of the vessels. Fixation can occur before 8–12h if decomposition is accelerated, or at 24–36h if delayed
by low temperatures.
The idea that it becomes fixed at 8–12h, is a generalization. It is possible to demonstrate that this "fixation" is not
defined by applying pressure to a discolored area and noting the subsequent blanching at the point of pressure.
Livor mortis may be confused with bruising, but bruising is rarely confused with livor mortis. Pressuring an area
of bruising will not cause blanching. An incision into an area of contusion or bruising shows diffuse hemorrhage.
In bruising, an incision into an area of livor mortis reveals the blood in vessels. Livor mortis also occurs internally,
with the settling of the blood in the dependent aspects of an organ (most evident in the lungs).
The pressure of the settling blood can rupture small vessels, with the development of petechiae and purpura. This
usually takes 18–24h and often indicates that decomposition is fast approaching. More common in asphyxial or
slow deaths. With time it cannot always be determined with certainty whether the purpura produced are ante or
postmortem. The presence of petechiae and purpura only in isolated areas suggests a postmortem origin. Petechiae
may develop even more rapidly in hanging limbs, appearing as early as 2–4 h after death.
Livor mortis can make interpreting head injuries in decomposed bodies harder. In a body lying on its back, blood
accumulates in the posterior or dependent half of the scalp due to gravity. In advanced decomposition, with lysis
of red blood cells and breakdown of the vessels, there is seepage of blood into the soft tissue of the scalp. This
gives the appearance of confluent bruising and cannot always be differentiated from true antemortem bruising.
, There won't be abrasion or laceration of the scalp, but all forensic pathologists have seen extensive scalp
contusions without abrasions or lacerations. In decomposed bodies, blood collecting in the occipital areas of the
brain due to gravity may escape through small vessels, producing very thin localized films of blood in the
subarachnoid or subdural spaces coating the occipital lobes. The rest of the brain does not show subarachnoid or
subdural hemorrhage.
In drownings where the body floats head down, decomposition produces the picture of diffuse scalp hemorrhage,
and postmortem minimal leakage of blood into the soft tissue of the anterior aspect of the neck may also occur.
Livor mortis is not very important in determining the time of death. It is important, however, in determining
whether the body has been moved.
2. Rigor mortis
Stiffening of the body after death, caused by the disappearance of adenosine triphosphate (ATP) from muscle.
ATP is the basic source of energy for muscle contraction, and it needs a continuous supply of ATP to contract
because the amount present is sufficient to sustain contraction for only a few seconds.
The three metabolic systems responsible for maintaining a continuous supply of ATP are the phosphagen system,
the glycogen–lactic acid system, and the aerobic system. The phosphagen system can provide maximal muscle
power for 10–15 sec, the glycogen–lactic acid system for 30–40 sec, and the aerobic system for an unlimited
period of time. After exercise, these three systems need time to be replenished. After death, the production of
ATP stops, but consumption continues. Without ATP, actin and myosin filaments become permanently
complexed and rigor mortis sets in. The complex remains until decomposition occurs.
Some factors that cause an important decrease in ATP prior to death are violent or heavy exercise, severe
convulsions, and high body temperatures, and it will speed up the onset of rigor mortis. It can appear within
minutes in some cases, and rarely, instantaneously (known as cadaveric spasm).
Cold or freezing will delay the onset of rigor mortis as well as prolong its presence. The rigidity can be “broken”
by passive stretching of muscles, after it is broken, it will not return. If only partial rigor mortis has set in prior to
stretching, then the residual unbroken rigor mortis can still set in. It usually appears 2–4h after death, and fully
develops in 6–12h (it can vary).
When rigor mortis develops, involves all the muscles at the same time and at the same rate. However, it becomes
most evident in the smaller muscles. It is said to appear first in the smaller muscles, such as the jaw, and then to
gradually spread to large muscle groups. The classical presentation in order of appearance is jaw, upper
extremities, and lower extremities (it passes off in the same order).
Rigor mortis is lost due to decomposition. In temperate climates, rigor mortis disappears in 36h, and it can last
up to 6 days. In hot climates, a body can be in a moderately advanced to an advanced state of decomposition in
24h, in which case, there will be no rigor mortis present.
Rigor mortis may be delayed or be very weak in emaciated individuals. Its onset may also be very rapid in infants.
Poisons, such as strychnine, that can cause convulsions can accelerate the development of rigidity. Any disease
or environmental factor that raises body temperature accelerates the development of rigor mortis. Hyperthermia,
loss of body regulatory temperature due to cerebral hemorrhage, and infection may accelerate the development
of rigor mortis.
The methods cited here are somewhat unreliable and inaccurate, usually giving vague or dubious answers. The
longer the time between death and the attempt to determine the time of death, the less precise the estimate of the
interval. The time the fatal injury has incurred is not necessarily the time of death.
Factors that can be used in determining the time of death:
1. Livor mortis
Lividity or postmortem hypostasis is a reddish-purple coloration in determined areas of the body due to the
accumulation of blood in the small vessels secondary to gravity. It can be misinterpreted as bruising by people
unfamiliar with this phenomenon. Dependent areas resting against a hard surface will appear pale in contrast to
the surrounding livor mortis due to compression of the vessels in those areas (no accumulation of blood). Areas
supporting the weight of the body (shoulder blades, buttocks, and calves) in individuals lying on their backs,
appear as pale areas. Tight clothing can compress soft tissues, collapsing the vessels, also producing pale areas.
Livor mortis usually has a cherry-red to pinkish color in deaths due to carbon monoxide, caused by
carboxyhemoglobin. That can also happen by exposure of a body to cold temperatures, and in deaths by cyanide.
Localized areas of bright red livor mortis are also seen adjacent to chest tubes. In all three of the aforementioned
entities, the coloration is caused by the predominance of oxygenated hemoglobin.
It is usually evident within 30 min to 2h after death. In individuals dying slowly, with terminal cardiac failure,
livor mortis may appear antemortem. Livor mortis develops gradually, usually reaching its maximum coloration
at 8–12h, when it is said to become “fixed”; before it will shift as the body is moved. If an individual dies lying
on his back, it will develop posteriorly on the back. If one turns the body on its face, blood will drain to the
anterior surface of the body, now the dependent aspect. It becomes “fixed” when shifting or drainage of blood no
longer occurs, or when blood leaks out of the vessels into the surrounding soft tissue due to hemolysis and
breakdown of the vessels. Fixation can occur before 8–12h if decomposition is accelerated, or at 24–36h if delayed
by low temperatures.
The idea that it becomes fixed at 8–12h, is a generalization. It is possible to demonstrate that this "fixation" is not
defined by applying pressure to a discolored area and noting the subsequent blanching at the point of pressure.
Livor mortis may be confused with bruising, but bruising is rarely confused with livor mortis. Pressuring an area
of bruising will not cause blanching. An incision into an area of contusion or bruising shows diffuse hemorrhage.
In bruising, an incision into an area of livor mortis reveals the blood in vessels. Livor mortis also occurs internally,
with the settling of the blood in the dependent aspects of an organ (most evident in the lungs).
The pressure of the settling blood can rupture small vessels, with the development of petechiae and purpura. This
usually takes 18–24h and often indicates that decomposition is fast approaching. More common in asphyxial or
slow deaths. With time it cannot always be determined with certainty whether the purpura produced are ante or
postmortem. The presence of petechiae and purpura only in isolated areas suggests a postmortem origin. Petechiae
may develop even more rapidly in hanging limbs, appearing as early as 2–4 h after death.
Livor mortis can make interpreting head injuries in decomposed bodies harder. In a body lying on its back, blood
accumulates in the posterior or dependent half of the scalp due to gravity. In advanced decomposition, with lysis
of red blood cells and breakdown of the vessels, there is seepage of blood into the soft tissue of the scalp. This
gives the appearance of confluent bruising and cannot always be differentiated from true antemortem bruising.
, There won't be abrasion or laceration of the scalp, but all forensic pathologists have seen extensive scalp
contusions without abrasions or lacerations. In decomposed bodies, blood collecting in the occipital areas of the
brain due to gravity may escape through small vessels, producing very thin localized films of blood in the
subarachnoid or subdural spaces coating the occipital lobes. The rest of the brain does not show subarachnoid or
subdural hemorrhage.
In drownings where the body floats head down, decomposition produces the picture of diffuse scalp hemorrhage,
and postmortem minimal leakage of blood into the soft tissue of the anterior aspect of the neck may also occur.
Livor mortis is not very important in determining the time of death. It is important, however, in determining
whether the body has been moved.
2. Rigor mortis
Stiffening of the body after death, caused by the disappearance of adenosine triphosphate (ATP) from muscle.
ATP is the basic source of energy for muscle contraction, and it needs a continuous supply of ATP to contract
because the amount present is sufficient to sustain contraction for only a few seconds.
The three metabolic systems responsible for maintaining a continuous supply of ATP are the phosphagen system,
the glycogen–lactic acid system, and the aerobic system. The phosphagen system can provide maximal muscle
power for 10–15 sec, the glycogen–lactic acid system for 30–40 sec, and the aerobic system for an unlimited
period of time. After exercise, these three systems need time to be replenished. After death, the production of
ATP stops, but consumption continues. Without ATP, actin and myosin filaments become permanently
complexed and rigor mortis sets in. The complex remains until decomposition occurs.
Some factors that cause an important decrease in ATP prior to death are violent or heavy exercise, severe
convulsions, and high body temperatures, and it will speed up the onset of rigor mortis. It can appear within
minutes in some cases, and rarely, instantaneously (known as cadaveric spasm).
Cold or freezing will delay the onset of rigor mortis as well as prolong its presence. The rigidity can be “broken”
by passive stretching of muscles, after it is broken, it will not return. If only partial rigor mortis has set in prior to
stretching, then the residual unbroken rigor mortis can still set in. It usually appears 2–4h after death, and fully
develops in 6–12h (it can vary).
When rigor mortis develops, involves all the muscles at the same time and at the same rate. However, it becomes
most evident in the smaller muscles. It is said to appear first in the smaller muscles, such as the jaw, and then to
gradually spread to large muscle groups. The classical presentation in order of appearance is jaw, upper
extremities, and lower extremities (it passes off in the same order).
Rigor mortis is lost due to decomposition. In temperate climates, rigor mortis disappears in 36h, and it can last
up to 6 days. In hot climates, a body can be in a moderately advanced to an advanced state of decomposition in
24h, in which case, there will be no rigor mortis present.
Rigor mortis may be delayed or be very weak in emaciated individuals. Its onset may also be very rapid in infants.
Poisons, such as strychnine, that can cause convulsions can accelerate the development of rigidity. Any disease
or environmental factor that raises body temperature accelerates the development of rigor mortis. Hyperthermia,
loss of body regulatory temperature due to cerebral hemorrhage, and infection may accelerate the development
of rigor mortis.
