Rigor mortis is one of the stages of death in which chemical changes that affect muscle fiber elasticity cause the muscles to stiffen. An indication of the time of death in forensic science, rigor mortis usually initiates at two to three hours after death and presents according to the position of the body at rigor mortis onset.
How Long Does Rigor Mortis Last?
How long rigor mortis lasts is of extreme importance to forensic scientists looking for a time of death or postmortem interval (PMI) when studying the body or the autopsy report. This is because the usual pattern of rigor mortis is possible to trace in time. Yet, certain factors such as the cause of death, temperature of the body or its environment, previous levels of fitness and muscle mass, drug abuse, infection, and availability of nutrients and ATP immediately previous to death can drastically shorten or lengthen these times. One medical report revealed rigor mortis onset and not cadaveric spasm as mentioned later on in this article, to occur within two minutes of cardiorespiratory arrest.
Most textbooks report that most cases of rigor mortis commence between two to three hours after death. Over the following twelve hours, rigor mortis set in, developing as myofibril chemical changes spread throughout every muscle. All muscle types – cardiac, skeletal and smooth – contain actin and myosin and all are therefore affected during the stage of rigor mortis. Maximum rigor mortis can continue for anywhere between 18 and 36 hours. As the next hours pass – sometimes days – these effects wear off. Muscles lose rigidity in the same order that they appear over the course of the next 24 – 50 hours.
Rigor mortis becomes even more pronounced if this natural course is broken. If, for example, a body is moved from its original position during the natural development of rigor mortis more significant rigidity may be the result. This is a very useful indication for forensic scientists looking for evidence of homicide or manslaughter where a body has possibly been moved from the scene after death.
In subjects who pass away when in a very low physical condition – usually very underweight and malnourished individuals – rigor mortis can set in much more rapidly. Muscle elasticity is dependent upon a source of energy in the form of adenosine triphosphate (ATP) but the amount of ATP stored in the muscles is only able to sustain a few seconds of muscle contraction. Once death has taken place, ATP synthesis halts but available resources continue to be consumed. Where low levels of ATP are present, either through time or absence of ATP, ATP non-availability and the acidic environment of a dead body due to lactic acid production cause the muscle-contracting proteins actin and myosin to bind together, forming a gel-like substance.
Rigor mortis initiates when ATP levels are approximately 85% of a normal, healthy level. In subjects who, previous to death, were unable to produce normal levels of ATP either through malnutrition or other disorders such as Huntingdon’s disease, rigor mortis will develop at a more rapid rate. In those with high muscle mass or high ATP production and transfer rates such as the active obese, rates can usually be expected to slow down. Adenosine triphosphate levels of 15% indicate maximum rigor.
It has been suggested that some bodies do not go through the process of rigor mortis at all. This idea is due to reports of lack of stiffness during the hours where rigor mortis is expected. As the chemical breakdown of actin and myosin is unavoidable after death, these reports are not accepted as proof of the absence of rigor mortis. Instead, it has been shown that the subjects in these reports were often very young children and babies with extremely low muscle mass. Rigor mortis would have been present in these individuals but the tactile method of measuring postmortem stiffness – manually bending the joints and evaluating the levels of resistance – gave results that did not point to a rigor mortis state. In other words, young limbs could be bent with little to no resistance due to low muscle mass. The claims of rigor mortis absence are therefore not accepted in the scientific community.
Rigor Mortis Stages
The stage of rigor mortis is third in an ordered group of postmortem phases known as the stages of death. The timescale a body needs to fully decompose depends on its pre-death anatomy, physiology, and the surrounding environment both at the time of death and after.
Rigor mortis follows stages pallor mortis and algor mortis respectively and precedes livor mortis. A full description of these stages continues below.
The Stages of Death
The stages of death often overlap. Pallor mortis is usually achieved within thirty minutes of death. Body cooling (algor mortis) initiates within this time and continues until the body is the same temperature as the ambient air – anywhere up to six hours postmortem. Muscle stiffening (rigor mortis) usually begins within one to two hours after a person has died and will continue for a number of days. Livor mortis begins at around the same time and requires approximately eight hours to progress to a maximum state. Autolyze or cell death also commences from the moment cell death occurs and continues throughout the fresh stage of decomposition; other early stages of decomposition are also present. All of these timescales depend heavily on the physiology and anatomy of the person and their immediate environment.
Pallor mortis or postmortem paleness is the result of the lack of capillary circulation once death has taken place and occurs almost immediately. This means pallor mortis is not a good indication of the time of death as bodies are often discovered at a later period.
The process of death begins upon what is known as somatic death. This is the cessation of cardiopulmonary activity and subsequent brain death. Once somatic death has taken place the supply of oxygen runs out and all cells die. This is called cellular death.
Pallor mortis accompanies cardiopulmonary activity cessation and brain death. However, one of the earliest indications of death in a clinical setting is the appearance of retinal vascular segmentation upon ophthalmoscopy where the cessation of circulation within the retina occurs at the start of the last stages of the dying process. This explains pre-death blindness.
A degree of pallor mortis is distinguishable whatever the skin color. The darker the skin, the weaker the effect but skin tone becomes paler in any newly dead organism. In the picture below, the difference between a normal hand and the hand of a person with anemia gives a good idea of what the color of skin in the stage of pallor mortis might look like.
The second stage of death is algor mortis or the cooling of the body. A body will naturally cool over the following two to three hours, although the variables relating to how slowly or how quickly a body cools down are multiple. The body remains pale. This occurs because of a lack of blood circulation but blood pooling can begin to give a slightly darker tinge to the skin of the lowest points of the body in relation to gravitational forces.
During algor mortis the body temperature lowers to match that of the surrounding environment and continues for approximately six hours postmortem. The rate of cooling is dependent upon the difference in body temperature and ambient temperature. This rate is increased in water, where a body is naked, and in the absence of high quantities of fat tissue. This means an obese, clothed body will cool down at a slower rate than a naked, thin body in a similar environment.
Rigor mortis, as already mentioned, is postmortem rigidity due to ATP depletion and lactic acid build-ups that form gel-like actin myosis bonds and keep the body in a certain position for up to fifty hours after death.
Previous to rigor mortis, muscles are flaccid. This flaccidity returns after the rigor mortis phase has ended. The first muscles visibly affected by rigor mortis are the eyelid, facial and jaw muscles. These are smaller muscles than those in the arms, legs, and trunk. Eventually, the breakdown by enzymes of actin and myosin binding sites during the last hours of rigor mortis initiates secondary, permanent muscle flaccidity.
Livor mortis or postmortem hypostasis indicates the pooling of blood in the blood vessels according to the forces of gravity. This results in darker skin in the lowest positioned tissues, usually the back of the head, shoulders, rump, and limbs when death occurs in a supine position.
Livor mortis begins approximately one-hour post mortem and develops over the course of three to four hours. By eight hours postmortem, livor mortis has progressed to its maximum state. Livor mortis is of extreme use to forensic scientists as lividity – skin changes associated with the pooling of blood once circulation has stopped – is a fixed entity. Even upon repositioning or relocation of the body, indications of its original position will remain.
Decomposition involves two different processes – autolysis and putrefaction. Autolysis begins immediately after cell death when cells begin to leak enzymes. This process is not visible to the eye and therefore often forgotten in death phase lists, replaced by the visible decomposition process of putrefaction.
Decomposition follows an order of stages, too. These are fresh, bloated, decay, post-decay and dry. An agreed group of decomposition stages has not yet been agreed upon in the world of scientific research. It is also impossible to take into account the range of intrinsic and extrinsic factors that affect the rates and appearance of decomposition.
Autolysis is present during the fresh stage of decomposition that begins upon cell death. Fresh decomposition lasts until around two hours postmortem as cells, starved of oxygen, die and lose their structure – a mechanism that occurs because of the build-up of lactic acid in the tissues. When the cell structure breaks down, its enzymes leak into surrounding tissues. Inside the digestive tract, still-living bacteria begin to consume the soft organs.
After autolysis comes putrefaction which describes the bloated, decay and dry stages of decomposition. The bloating period begins after dead cells have broken down and is one of the first visible signs of the decomposition process. The bacteria within the body produce gases which the non-breathing corpse cannot diffuse. The tongue and eyes may protrude and the smell of death becomes noticeable. Bloating usually begins around the second-day postmortem and continues for a further five to six days.
The decay phase continues on from the end of the bloating phase and lasts for approximately eleven days. Bacteria-produced gases escape creating a strong, putrid smell that is attractive to decomposers. The corpse takes on a wet appearance as fluids drain via orifices and pores. Inside the body, organs are well decomposed, helping to produce the aforementioned fluids.
Post decay begins at around the tenth to twelfth-day postmortem. Where insects, fungi, and bacteria are present, such as in or on the soil, most of the flesh will have been consumed or is decomposed by this point. This is why this stage is sometimes referred to as skeletonization.
Finally, dry stage decomposition that begins at about three to four weeks after death involves the decomposition of dry remains, usually bones, cartilage, and dehydrated skin. Some products such as adipocere or ‘corpse wax’ composed of fatty acids may need considerable time to break down.
What Causes Rigor Mortis?
Rigor mortis causes require an understanding of muscle contraction mechanisms in the living organism.
When action potentials sent via the nerves reach their target muscles, calcium ions are released from muscle transverse tubules which make up a part of the sarcoplasmic reticulum. The sarcoplasmic reticulum that surrounds each myofibril within a muscle fiber is responsible for calcium ion concentration in the muscle fiber. In a resting muscle fiber, the cytosol is practically free of calcium ions as the sarcoplasmic reticulum ‘sequesters’ them away, binding them to a protein called calsequestrin. There is more calsequestrin in fast-contracting muscle fibers than in slow-contracting fibers.
When an impulse is sent by the nervous system to ask a muscle fiber to contract, the transverse tubules that travel from the surface of each fiber forward this impulse whenever the tubules come close to the sarcoplasmic reticulum. In the presence of such a signal, any area of the sarcoplasmic reticulum close to the transverse tubule will release calcium ions.
The released calcium ions cause troponin and tropomyosin to move along the muscle filament; this action initiates muscle contraction. After the muscle has contracted (and in the absence of further signals from the nervous system) the leftover signaling neurotransmitter, acetylcholine, is broken down by acetylcholinesterase.
The SERCA pump (sarcoplasmic endoplasmic reticular calcium ATPase pump) stops releasing calcium ions and sequesters them off to quarantine areas within the sarcoplasmic reticulum. The lack of available calcium ions blocks the movement of myosin and the muscle is able to relax. Only constant nervous system signals can keep a muscle contracted for any length of time in the living body. In the dead, no nervous system signals are present due to brain death and muscle contraction is then solely the result of chemical imbalance.
As its full name suggests, a SERCA pump requires plentiful ATP. After death, all metabolic activity ceases to function and ATP is no longer produced. This leads to permanently elevated calcium ion levels within the sarcomere and no sequestering mechanism. The SERCA pump is, therefore, unable to remove them. The result of this is sustained contraction or rigor mortis.
What is Cadaveric Spasm?
A cadaveric spasm is quite rare. When rigor mortis commences at an extremely accelerated rate it is renamed cadaveric spasm, instant rigor, postmortem spasm or cataleptic rigidity. The cadaveric spasm occurs in the absence of primary muscle flaccidity and is most commonly encountered in deaths that involve serious physical and/or emotional stress.
A cadaveric spasm usually affects a single group of muscles such as those of one limb or hand. Cadaveric spasm is probably the result of the combination of neurogenic mechanisms and high muscular exertion immediately prior to death. Examples include dead bodies tightly gripping weapons or objects of defense, blades of grass, and precious possessions. Cadaveric spasms are most common in violent situations such as war and brawl scenarios, and modes of death like falling, drowning, and plane crashes.