Post mortem primary changes

These are those that occur first and continue until the appearance of the first signs of cadaveric putrefaction.

Cadaveric dehydration

The ocular, buccal and genital mucous membranes, as well as the skin, undergo a natural drying process by evaporation. After death, they become dry, opaque and easily become darker in color than normal tissue. In addition, skin that is in contact with air dehydrates more rapidly than those areas that are resting on surfaces, which have a greater tendency to macerate (soften). The speed of these processes depends on environmental temperature, humidity and ventilation.

In addition, corneal opacity occurs, in which the eyeballs retract (sinking of the eyeball) and corneal desiccates (the cornea becomes no longer transparent).

Algor mortis or cadaveric cooling

This is a physical process in which the cooling rate of the cadaver is determined by the difference between the cadaver temperature and that of the environment. That is, the temperature of the cadaver tends to equilibrate with that of the surrounding environment. This phenomenon occurs mainly by convection and radiation. If the cadaver is wet, evaporation becomes a more important factor.

This factor is one of the most important during the first hours after death in order to establish the "postmortem interval", the PMI being the estimate of how long the subject has been dead.

The temperature factor is only applicable within the first 24 hours postmortem. During the first 1-5 hours the temperature remains stable (thermal plateau). After this time, there is a linear decrease in heat loss, being faster the closer to room temperature.

It should be noted that this cadaveric cooling curve is not an exact or absolute indicator of the time of death or IPM. It is a relative indicator that has to be taken into account together with the rest of the factors that influence the speed of appearance of postmortem alterations (body size, body condition, external surface, species, breed, type of disease that caused death, temperature, humidity of the environment, etc.).

It is important to take into account that the animal before death may have presented a body temperature outside normal parameters (above or below normal, i.e. fever or hypothermia).

Rigor mortis or cadaveric rigidity

First, a very brief total muscle relaxation (primary muscle flaccidity) occurs as a consequence of the cessation of central nervous system (CNS) activity. This relaxation is characterized by pupillary dilatation, relaxation of the organs with muscular wall and sphincters, as well as total muscular flaccidity in the limbs and body.

This is followed by a generalized rigidity of the entire musculature of the organism (contraction of the musculature) which prevents the mobilization of the joints. This phenomenon is called rigor mortis or cadaveric rigidity.


Adenosine triphosphate (ATP) is necessary for muscle contraction and relaxation to occur under normal conditions. This molecule provides the energy necessary for calcium to return to the muscular sarcoplasmic reticulum and for the actin and myosin molecules to separate (relaxation).

ATP synthesis is produced by 3 metabolic pathways: two of them anaerobic (glycolytic anaerobic-anaerobic lactic anaerobic system and phosphagen-anaerobic alactic system) and a third aerobic (oxidative-aerobic system).

After death, and with the cessation of blood circulation, the muscle fibers begin a period of anoxia (lack of oxygen), which implies a decrease in ATP synthesis and activates the non-oxygen-dependent metabolic pathways in order to synthesize ATP. Anaerobic glycolysis is therefore initiated, resulting in the rapid depletion of muscle glycogen and the intracellular increase of pyruvic and lactic acid. These metabolic by-products cannot be removed due to the lack of blood circulation, so they are retained in the intracellular space. The end result is a drop in intracellular pH from pH 7 to pH 5.6 along with a drop in Adenosine-Triphosphate (ATP), which blocks the binding of actin and myosin (muscle proteins) preventing myosin from separating from actin until breakdown breaks them apart. The muscle remains in a permanent contraction because there is no energy for calcium to return to the sarcoplasmic reticulum and separate the actin and myosin molecules.

The decrease in pH and the presence of free calcium in the sarcoplasm activates the cathepsin enzyme system, thus initiating a new phenomenon, autolytic proteolysis, i.e. the action of endogenous enzymes on actin and myosin molecules, together with the action of exogenous enzymes (of bacterial origin), whose combined action leads to the denaturation of muscle proteins. At this point, the phase of secondary muscular flaccidity or termination of cadaveric rigidity begins.

The total disappearance of stiffness coincides with the onset of putrefactive phenomena.

How can the onset and duration of rigor mortis vary?

Muscle size. This stiffness is characterized by the fact that it occurs progressively in all muscles at the same time, but first in those muscles of small size, mainly in the jaw

Forced rupture of the actin-myosin junctions. Rigor mortis can be forced to cease by stretching the limbs with force, preventing rigor mortis from reappearing if it was already fully established. If this is done before rigor mortis has fully developed, it will reappear, although the rigidity will be less than expected. Therefore, it is important to know how the cadaver was handled and transported in order to establish the PMI correctly.

Sometimes rigor mortis appears immediately after death (cadaveric spasm), as for example in cases of electrocution.

Environmental temperature

  • In temperate climates, the rigor mortis cycle lasts approximately 36-48 hours.
  • In warm climates, the rapid onset of putrefaction causes rigor mortis to disappear in about 12 hours (shortening of rigor mortis onset time and rigor mortis duration).
  • In cold climates, the onset is delayed, with the total duration of the cycle being longer. At temperatures averaging below 10°C, cadaveric rigidity rarely develops.

Degree of muscular activity prior to death

Rigor mortis is of rapid onset and very short duration in (glycogen levels):

  • Animals with prolonged fasting or intense pre-death activity, such as capture stress, or in diseases with intense muscle contractures such as tetanus, meningoencephalitis, etc.
  • Young animals, compared to adults.
  • Animals affected by catechizing or septicemic diseases.

Rigor mortis is of late onset and development in:

  • Carcasses with low external temperature.
  • Animals with "sudden death" (thought to be associated with the lack of previous muscular activity in this form of somatic death).
  • Deaths caused by: asphyxia, carbon monoxide poisoning.
  • Animals with anemia, due to severe hemorrhages.

It is important to differentiate rigor mortis from:

  • Animals subjected to intense heat (direct fire) whose stiffness is caused by coagulation of muscle proteins, and not by rigor mortis itself.
  • Cold and freezing also causes muscle stiffness and postpones the true development of cadaveric stiffness.

Extent of rigor mortis development

The degree of development of rigor mortis within the cadaver should always be assessed at the initial examination or inspection of the cadaver prior to necropsy, which may be: complete, partial or absent.

The way to evaluate it is to try to flex the different joints: the stiffness of these will indicate the location and degree of development of rigor mortis.

The order of involvement of the different muscles proceeds as follows (from the earliest to the latest):

  1. Smooth musculature of the gastrointestinal organs.
  2. Small muscles of the eyelids, lower jaw and neck.
  3. Extremities: from distal joints to large proximal joints.

Generally, rigor mortis disappears in the same order in which it started and developed, i.e. sequentially. Although this fact is not constant, symmetrical or regular, it is thought that the development is simultaneous in all the musculature, but that it takes longer to settle definitively in the large muscle masses than in the small ones.

Use of rigor mortis to estimate PMI

Using rigor mortis as a method to estimate the time of death or PMI is not very reliable, but it is possible to estimate this interval according to:

  • Cadavers that are still warm and rigor mortis is not present: death occurred within the previous 3 hours.
  • Bodies in which the rigor mortis is in process: death occurred between 2 and 9 hours prior to finding.
  • Cadavers in which rigor mortis is fully established: death occurred approximately 9 to 12 hours before.

Bodies in which the temperature is in equilibrium with that of the environment and the rigor mortis is beginning to disappear, but there are still no signs of putrefaction: death occurred approximately 24-36 hours ago.

Livor mortis or cadaveric hypostasis

This is the accumulation of blood in certain declined areas of the cadaver due to the effect of gravity after the heart has stopped beating. In addition to gravity, the fact that the blood remains in a liquid state for a certain period of time allows sedimentation in declined areas of the bodies. Subsequently, blood coagulation will occur, followed rapidly by the release of fibrinolysin, which will dissolve the clots, especially at the capillary level and in small vessels. In this way, gravitational recirculation is favored.

These areas acquire a red to blue coloration due to the loss of oxygen from the blood and mixing with deoxygenated venous blood. At the onset of putrefaction, these areas change by putrefactive degradation of hemoglobin, first taking on a green color (sulphohemoglobin) and then brown-black, by a process of post mortem imbition.

Different colorations can be found depending on the cause of death:

  • If death was caused by carbon monoxide poisoning, they take on an intense-red coloration.
  • If death was caused by methemoglobin-forming poisons, these areas take on a brownish-red color.

In addition, the manner of preservation can affect this process:

  • In refrigerated or frozen bodies, they usually appear as bright pink areas.

It is very important to distinguish livor mortis from:

  • Cyanosis, an antemortem process that results in a bluish coloration of the mucous membranes.
  • Hematomas: the blood is not confined to the blood vessels, but is diffusely distributed in the soft tissues. If it is a hematoma, if pressure is applied to that area, the blood will not be displaced and no blanching of the blood will be seen. You can also try to wash it after cutting that region, if the blood is not removed, it means it is a hematoma.

Livor mortis in cadavers may be noticeable 3-4 hours after death, stabilizing in 8-12 hours. After the first 24 hours of after death it no longer occurs.

This coloration may appear more rapidly in accelerated decomposition or in diseases characterized by failure of the general circulation, or appear more slowly with cold environmental temperatures or with hemorrhagic or anemia-causing diseases, stabilizing at 24-36 hours after death.

Livor mortis can be determined to have stabilized when there is no further movement or drainage of blood because blood has left the vessels as a result of hemolysis and degradation of the blood vessel walls by decomposition. If no blanching occurs when pressure is applied to the area, livor mortis has stabilized.

Cadaveric livor mortis is a useful tool during postmortem inspection to determine the position of the cadaver at the time of death and whether or not the cadaver has been moved. A number of aspects should be taken into account:

  • The declined areas of the bodies that suffer pressure against firm surfaces do not have livor mortis due to compression of the blood vessels, as it prevents the filling of the vessels. This fact can be applied to any material or device that constrains the body, which will reveal the pattern related to the item that was used on the body.
  • After the first 12 hours after death, livor mortis become "fixed". If the cadaver is moved, the blood is redistributed, but the primary distribution does not discolor, always leaving its mark. If the cadaver is moved during the first 6 hours, livor mortis discolor and a new secondary distribution develops.

Organic hypostatic

This is a change in coloration of the lower parts of the organs, which turn a red color more intense than normal, while the upper part maintains its color or looks paler. It is due to the accumulation of non-circulating intravascular blood located in organs (lungs, liver, kidneys and intestines).

It should not be confused with a true congestion or inflammation, since in these cases the affected area would not be related to the postmortem position of the organ.

Postmortem autolysis

Decomposition involves two processes: autolysis and Putrefaction. Autolysis is a chemical process of degradation of tissues and organs (healthy or altered) due to intracellular enzymes in the cadaver. That is, it results from the action of lysosomal hydrolases released into the cytoplasm of cells together with the action of enzymes produced in other cells and released into the medium by the increased permeability of cell membranes undergoing anoxia.

These internal and external enzymatic reactions result in the complete dissolution of cellular structures. Finally, the cell will undergo its own lysis and dissolution.

It is very important to know how to differentiate this process from others both grossly and microscopically. Grossly, autolysis of tissues and organs, is characterized by:

  • Loss of color: Loss of color: autolytic tissue is uniformly pale. Intravascular hemolysis of red blood cells engulfs the tissue giving rise to a uniform black-red color. It is important to differentiate this shade from that produced by antemortem changes. Antemortem changes usually have a defined or focal distribution, whereas autolytic changes are usually uniformly distributed throughout the organ.
  • Loss of resistance: Autolytic tissues are not very resistant to pressure or tension as, for example, is the case of the intestine that ruptures during handling or in the case of solid organs (liver, spleen, kidney) that increase their fragility.

Microscopically, it is possible to differentiate whether it is an autolytic process or necrosis.

  • Antemortem changes are characterized by a focal or patchy distribution (although this is not always the case), they are accompanied by hyperemia or inflammatory reaction surrounding the necrotic focus, so that an approximation can be established between the time of appearance of the lesion and death.
  • Postmortem autolysis is generally distributed throughout the affected tissue, intravascular erythrocytes show a loss of contour and coloration, and intravascular hemolysis can also be found.

There are different factors that condition the speed of onset of autolysis such as:

  • Temperature: Heat accelerates autolysis, and cold slows it down. Freezing can stop the autolysis process, and in some cases significant heat can inactivate enzymes that are rapidly inactivated.
  • Type of tissue: Tissues that have cells with a high content of hydrolytic enzymes (pancreas, liver, kidney, digestive tract) undergo autolysis more rapidly. Other tissues that undergo rapid autolysis are: the mucosa of the gallbladder, the adrenal medulla, the neurons of the nervous tissue and the proximal convoluted tubules of the renal cortex. In those tissues constituted by cells with low enzymatic contents (connective tissue, muscle, bone, etc.), autolysis will occur more slowly.
  • Characteristics of the animal: Large amount of hair, high state of greasiness, high body temperature (fever), septicemic conditions, etc. These facilitate heat retention and thus accelerate the autolysis process.

Destruction of the cadaver by exogenous factors

Among the exogenous factors that can vary the conditions of the cadaver are: environmental conditions, flora and fauna, and anthropogenic causes.

It has to be know how to differentiate all these alterations from the signs of a real antemortem injury. An antemortem lesion will present gross and microscopic signs such as: hematic infiltration of the edges, retraction of the edges, turgor, congestion and tissue edema, perilesional capillary rupture and inflammatory infiltrate surrounding the lesion.