Rigor Mortis

Rigor mortis is defined by the decline of ATP to zero, 0% extensibility, an ultimate pH that is reached, and the production of lactic acid that has plateaued.

From: Encyclopedia of Food and Health , 2016

Postmortem Changes: Overview

M. Tsokos , R.W. Byard , in Encyclopedia of Forensic and Legal Medicine (Second Edition), 2016

Medicolegal Aspects

Rigor mortis is occasionally helpful in determining whether a body has been moved after death. If a body is found in an unusual position – for example, one that could not have been maintained under the influence of gravity during primary relaxation of the muscles after death – this position implies that the body has been moved after the development of rigor mortis.

Rigor mortis may make examination of the palms and inner aspects of the fingers difficult, so that current marks or defense injuries located here may be overlooked.

Marked anal dilatation may be observed postmortem, particularly in children. As previously mentioned, when death occurs and preceding the onset of rigor mortis, the whole body musculature loses its tone. In children, rigor mortis may fix a dilated anal orifice, and this finding may persist after rigor mortis has faded. Anal dilatation is not, therefore, a sufficient marker of penetrative anal abuse.

Muscle relaxation immediately after death with opening of the eyes and mouth and subsequent fixation in rigor mortis often occurs after death, giving the face the appearance of grimacing. However, despite common beliefs, the face of a decedent does not reflect whether the individual's last moments were of fear or fright.

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POSTMORTEM CHANGES | Overview

M. Tsokos , in Encyclopedia of Forensic and Legal Medicine, 2005

Criminalistic Aspects

Rigor mortis is occasionally helpful in determining whether a body has been moved after death. If a body is found in an illogical posture, such as a body position that would not have been maintained under the influence of gravity during primary relaxation of the muscles after death, this position implies that the body has been moved after the development of rigor mortis.

Rigor mortis may make examination of the palms and the inside aspects of the fingers difficult so that current marks or defense injuries located here may be overlooked.

Particularly in children, a marked anal dilatation may be observed postmortem. As mentioned before, immediately as death occurs and preceding the onset of rigor mortis, the whole body musculature loses its tone. In children, rigor mortis may fix a dilated anal orifice and this finding may persist after rigor mortis has faded. Therefore, anal dilatation alone is not a sufficient marker for penetrative anal abuse before death.

Muscle relaxation immediately after death with opening of the eyes and the mouth and subsequent fixation in rigor mortis often occurs after death, giving the face the appearance of grimacing. However, despite common belief, the face of a deceased does not reflect whether the individual's last moments were of fear or fright.

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Forensic Taphonomy

Amy E. Rattenbury , in Forensic Ecogenomics, 2018

Rigor Mortis

Rigor mortis is possibly one of the most well known of the taphonomic changes and is the process that causes the muscles in the body to stiffen resulting in rigidity due to a range of chemical changes in the muscle structure. Muscle fibers, which in life move because of sliding filament theory, rely on the conversion of ATP to ADP. After death, when respiration ceases, the intracellular pH decreases due to the production of lactic and pyruvic acid. The anaerobic glycolysis of glycogen in the muscles causes glycogen depletion and thus reduced ATP concentrations. Also calcium leaks into the sarcomere, where the protein filaments of actin and myosin are present in an alternating arrangement, where calcium then binds allowing for a cross-linkage to occur between the filaments. This causes a pulling motion along the length of the muscle causing it to become shorter and more rigid. In a living individual, ATP would be used to dissociate the cross-linking in the fibers and as a result the rigidity associated with the change would be reversed, whereas it becomes fixed postmortem (Powers, 2005).

First noticed in the small muscle groups such as in the hands and face, rigor can take hold within 3 to 4   h and normally extends across the large muscle groups also within the first 12   h after death, causing the entire body to become stiff. Variations in this time period are observed particularly in individuals who may have decreased levels of ATP at the point of death. This could be caused by exercise or strenuous activity in the perimortem period around the time of death (Madea, 2015). Rigor mortis can also be helpful in the reconstruction of the postmortem period by preserving the positioning of the body and in some circumstances showing if any attempt has been made to move the body. However, this type of interpretation is very much time dependent and relies on rigor still being present at the time the body is discovered. The point at which this rigidity reverses and the stiffness passes is extremely variable because of significant differences in the volume of muscle in the remains. However, the body generally returns to a fully flaccid state after 36   h from the time of death, although this can increase by up to 10   days in refrigerated remains (Varetto and Curto, 2005). The exact cause of the breakdown on the cross-linked bonds is not well established, although it is generally credited to enzyme action and the increased cellular breakdown occurring throughout the body.

Since rigor mortis occurs in a somewhat predictable pattern, it has been suggested that it can be used to estimate the PMI in combination with body temperature. Knight and Saukko (2004) presented a timeline allowing for bodies categorized as stiff/flaccid and warm/cold to be dated as dead for less than 3   h, 3–8   h, 8–36   h, and more than 36   h. However, due to the variations in both algor and rigor mortis this method is best not used for anything more than a primary indication.

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Materials and methods

Jarvis Hayman MB,ChB, FRCS(Ed), FRACS, MA(Hons) Archaeology, PhD , in Estimation of Time Since Death in Australian Conditions, 2021

3.2.4.1 Decomposition of the external body surface

Rigor mortis may still be present or just waning. The body is at ambient temperature. The skin is pallid. There is no bloating present. (1 point)

Rigor mortis is absent. Livor mortis is present except over pressure areas but is not fixed, as it blanches on pressure. The skin over the lower right abdomen is slightly green. Focal marbling and bloating are beginning. Fluid purging from mouth and rectum is beginning. (2 points)

Livor mortis is patchy or widespread and fixed. Green discolouration of the abdomen is becoming more widespread. Skin blistering is apparent and there may be some skin slippage, but it is not yet widespread. Abdominal and generalised bloating is at its maximum. Focal marbling and purging are now profuse. Facial features are obscured by bloating and a darkening colour. (3 points)

Livor mortis has been obscured by a more generalised green, purple or brown colour or a patchy mixture of all three. Bloating is still present but is receding. There is widespread skin slippage and peeling. Marbling is at its fullest extent and may still be visible. Drying of the peripheries is occurring, that is the fingers, toes, ears and nose. The orbits are sunken and the eyes soft, shrunken and the details obscured. The hair and fingernails are easily avulsed. (4 points)

The skin colour has darkened to a predominantly black colour and is widespread. Bloating has receded and the abdomen is now scaphoid. The skin is of a parchment texture and dry. There may be mummification of the digits. The hair and nails have become avulsed. There may be areas of mould or microbial growth and superficial patchy skin and tissue loss caused by insects. (5 points)

Much of the skin and soft tissue is lost. The internal organs may be exposed and either absent or shrivelled and dry. There may be mummification of residual tissue. Bones of the thoracic cage, limbs and pelvis may be exposed. The cranium may be disarticulated in the cervical region. (6 points)

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Estimation of Time since Death

Ranald Munro BVMS, MSc, DVM, Dip Forensic Medicine, DipECVP, MRCVS , Helen M.C. Munro BVMS, MRCVS , in Animal Abuse and Unlawful Killing, 2008

Rigor mortis

Fully developed rigor mortis is an easily identifiable and reliable indicator that death has occurred. The time of onset is variable but it is usually considered to appear between 1 and 6 hours (average 2–4 hours) after death. Depending on the circumstances, rigor mortis may last for a few hours to several days.

The muscles of the face and neck are often the first to be affected and the rigidity spreads backwards over the trunk and limbs. Relaxation of the muscles occurs in roughly the same order. Contraction of the heart is an early and forceful change. In the healthy, non-hypoxic animal the left ventricle expels virtually all its contents of blood during this process, whilst contracture of the right ventricle is less intense, leaving a small quantity of clotted blood in this chamber.

The development and resolution of rigor mortis is complex, the rate of onset being greatly influenced by the glycogen content of muscle, the pH of muscle and the temperature. Adenosine triphosphate (ATP) is a necessary component in the relaxation of the myosin filaments of normal muscle. Rigor mortis commences when the rate of re-synthesis of ATP is less than its degradation. In the early hours after clinical death, muscle glycogen fuels the cycle of hydrolysis and re-synthesis of ATP. Consequently, ante-mortem events that reduce glycogen stores (e.g. hunting) can result in the rapid onset of rigor mortis. In contrast, 9–12 hours may elapse after slaughter of well fed, well rested cattle before the onset of rigor mortis.

Body temperature also affects the rapidity of onset. The most dramatic example is the onset of rigidity within minutes in cases of malignant hyperthermia. 10, 11 Following fatal hyperthermia of dogs in vehicles, less than 1 hour may pass before rigor mortis is recognisable and it may spread rapidly throughout the muscle groups. Raised body temperature as a consequence of severe exercise may also significantly shorten the time before rigor mortis develops.

However, the effects of increased body temperature are not always so clearcut and the presence of systemic disease must be considered. Whilst pyrexia caused by acute fatal infectious disease may result in rapid onset of rigor mortis, fevered animals with high muscle pH may show delayed rigor mortis or may not develop rigidity at any stage.

In general, high environmental temperature will accelerate the onset, whereas low ambient temperatures have the opposite effect. The duration of rigidity is extended in dry cold conditions. Although the details of the relaxation process are not clear, it is generally accepted that the dissolution of rigidity is associated with early decomposition or denaturisation of muscle.

For the veterinarian, a further complication is the, as yet, largely undocumented variation in the times of onset and disappearance of rigidity that may exist among species and ages of the broad spectrum of animals presented for examination. As a result of these variables, it is prudent to consider rigor mortis as providing only a rough guide to the post-mortem interval.

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Tissue Biochemistry

John W. Pelley PhD , in Elsevier's Integrated Biochemistry, 2007

Energy Sources

Because muscular contraction can become quite intense, the short-term demands of the muscle cell can exceed the energy provided by normal fuel metabolism. Two main enzymes create short-term supplies of ATP: creatine kinase and adenylate kinase (myokinase).

Creatine phosphate is formed by phosphorylation of creatine with ATP catalyzed by creatine kinase (Fig. 20-4). This reaction is reversible, allowing rapid generation of ATP from creatine phosphate and ADP. During normal metabolism, the ample supply of ATP favors the formation of creatine phosphate, which then acts as a storage battery, ready to regenerate ATP when ADP accumulates.

PATHOLOGY

Rigor Mortis

Subsequent to a person's death, metabolism becomes anaerobic with the depletion of ATP. Since ATP is needed to bind to myosin and release it from the actin filament, the myosin remains bound in the contracted state. When this final state occurs in all of the myofibrils, the muscle fiber enters a state of constant contraction.

Adenylate kinase can combine two ADP molecules to produce one ATP and one AMP. This squeezes all the energy available from ADP supplies once the creatine phosphate has been depleted. During normal metabolism, the ample supply of ATP favors the restoration of ADP, which then undergoes oxidative phosphorylation to ATP.

Lactate dehydrogenase (LDH) isoenzymes are different in heart and skeletal muscle, reflecting their different metabolic requirements. Heart is an aerobic tissue and is adapted to use lactate as a fuel, whereas skeletal muscle can experience temporary anaerobic conditions and is adapted to produce lactate under those conditions. LDH is a tetramer of four catalytic subunits; there are two types of subunits: heart (H) and muscle (M). The five possible LDH isoenzyme tetramer combinations are H4, H3M, H2M2, HM3, and M4H.

Skeletal muscle has more M subunits expressed, which produces more HM3 and M4 tetramers. The M subunit has a high affinity for pyruvate, favoring the production of lactate (pyruvate → lactate) under anaerobic conditions. Some lactate is produced, even at rest.

Heart muscle has more H subunit expressed, which produces more H4 and H3M tetramers. The H subunit has a higher affinity for lactate and is inhibited by pyruvate, favoring production of pyruvate (lactate → pyruvate) for aerobic metabolism.

KEY POINTS ABOUT MUSCLE CONTRACTION AND ENERGY SOURCES

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Muscle contraction involves a change in the physical relationship between actin filaments and myosin-ADP-Pi complexes; the power stroke involves a conformational change in the myosin head groups when ADP dissociates.

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Muscle contraction relies on creatine phosphate and adenylate kinase to maintain ATP concentrations; the energy needs of heart and skeletal muscle are reflected in their lactate dehydrogenase isozyme composition.

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Hypothermia

John A. Marx MD , in Critical Care Secrets (Fourth Edition), 2007

5 In the field, what are the indications to initiate cardiopulmonary resuscitation (CPR) in a patient with suspected hypothermia?

Apparent rigor mortis and lividity are not necessarily reliable indicators in severe hypothermia. Pupils can be fixed and nonreactive at temperatures below 22°C. Peripheral pulses are difficult to palpate in patients with profound bradycardia and vasoconstriction. At least 45–60 seconds should be spent in determining whether spontaneous pulse is present because even extreme bradydysrhythmias may be sufficient to meet the very depressed metabolic needs of a hypothermic patient. A Doppler device or ultrasound can assist in determining whether a pulse or cardiac activity, respectively, is present. Moreover, unnecessary handling, including closed chest compressions, is a purported cause of arrhythmias, although definitive evidence for this is lacking. If no evidence of perfusion can be discerned, an arrest rhythm should be presumed and CPR initiated. Respiratory minute volume is also significantly depressed, and careful scrutiny is required to distinguish apnea. A patent airway should always be established, and if the patient is in respiratory arrest, ventilation should be instituted. Endotracheal intubation does not cause dysrhythmias.

CPR in hypothermia is contraindicated under any of the following circumstances: (1) any signs of life are present, (2) lethal (non–hypothermia-related) injuries are obvious, (3) chest wall compression is impossible due to loss of elasticity, (4) "do not resuscitate" status is verified, or (5) the lives of the rescuers are endangered by environmental conditions.

It may be difficult to distinguish primary from secondary hypothermia (e.g., the patient who dies of cardiac arrest in a cold environment). The oft-quoted maxim that a patient is not dead until warm and dead provides an appropriate caution. Physician judgment is needed, however, to help determine when to begin or cease CPR.

Danzl DF, Pozos RS, Auerbach PS, et al: Multicenter hypothermia survey. Ann Emerg Med 16:1042–1055, 1987.

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Supravital Reactions in the Estimation of the Time Since Death (TSD)

Jarvis Hayman , Marc Oxenham , in Human Body Decomposition, 2016

Rigor Mortis

The phenomenon of rigor mortis was first described in 1811 by the French physician, P.H. Nysten, but its physiological basis was not discovered until 1945 by Szent-Györgyi (2004). It consists of a sustained contraction of the muscles of the body, which begins at 2–6   hours after death, persists for 24–84   hours, and is then followed by gradual relaxation until the muscles again become flaccid (Gill-King, 1997). The contractile units of muscle cells, sarcomeres, consist of parallel units of two types of protein, actin and myosin. Crosslinkages on the myosin units pull the actin units toward each other, causing muscle contraction. The process requires calcium and energy, the latter provided by adenosine triphosphate (ATP) (Bate-Smith and Bendall, 1947). The initial flaccidity of muscles after death is due to continued formation of ATP by anaerobic glycolysis, but with the passage of time, ATP is no longer resynthesized, energy is no longer available for the actin and myosin fibrils to remain relaxed and the fibrils contract, resulting in the muscle body as a whole contracting. Resolution of rigor mortis after 24–84   hours is caused by proteolytic enzymes within the muscle cells disrupting the myosin/actin units, causing the crosslinkages to break down and the muscles to relax (Gill-King, 1997).

At the beginning of the 19th century Nysten (1811), in France, carried out experiments on criminals immediately after their decapitation on the guillotine and he observed that rigor mortis began in the muscles of the jaw and then progressed distally to the feet and toes. This sequence was disputed by Shapiro (1950, 1954), who suggested that it began at the same time in all muscles but the variation in the sizes of the different joints and muscles meant that the larger muscles took longer to develop rigor mortis, giving the impression that it progressed from proximal to distal in the body. Krompecher designed an experiment to measure the intensity of rigor mortis in rat front limbs compared with rat hind limbs using different forces at different times during the course of rigor mortis (Krompecher and Fryc, 1978a). The hind limbs had a muscle mass 2.89 times the muscle mass of the front limbs. The results showed that although there was no difference between front and hind limbs with respect to the time taken to reach complete evolution of the rigor mortis, the onset and the relaxation of rigor mortis were more rapid in the front limbs which had the smaller muscle mass. In contrast, Kobayashi and colleagues (2001), experimenting with in vitro rat erector spinae muscles, found that although the volume of muscle samples varied there was no difference in the development and resolution of rigor mortis. They concluded that it was the proportion of muscle fiber types in each muscle, difference in temperature, and the dynamic characteristics of each joint that determined the speed of onset and resolution of rigor mortis.

Several intrinsic and extrinsic factors affect the speed of onset and duration of rigor mortis. Intrinsic factors such as violent exercise and high fever during the agonal stage will cause a rapid onset and shorter duration. The amount of skeletal muscle dictates the duration of rigor, for example, it appears and resolves early in infants but, in contrast, a robust physical person will have slower onset and a prolonged duration (Gill-King, 1997). This finding, however, was contradicted by Kobayashi and colleagues (2001). Krompecher and Fryc (1978b), in a study using rats, found that physical exercise before death caused an increased intensity of the rigor which reached its maximum intensity at the same time as normal controls but the maximum intensity was sustained longer. The rigor, however, reached resolution at the same time as the controls. In a controlled experiment using rats, Krompecher (1981) found that the higher the temperature, the shorter was the onset of rigor and the faster the resolution, a finding later confirmed by Kobayashi and colleagues (2001). At very low temperature (6°C), development was very slow at 48–60   hours and resolution very prolonged to 168   hours. This contrasted with a temperature of 37°C when development occurred at 3   hours and resolved at 6   hours. In a mortuary where corpses were kept refrigerated at 4°C, rigor was found to completely persist for 10 days in all corpses, became partial by 17 days, and resolved after 28 days (Varetto and Curto, 2005).

Other extrinsic factors which affect the course of rigor mortis are electrocution causing death, which accelerates the onset of rigor and shortens the duration, possibly because the violent cramps experienced cause a rapid fall in ATP (Krompecher and Bergerioux, 1988). Strychnine poisoning hastens the onset and duration of rigor mortis while carbon monoxide poisoning delays the resolution (Krompecher et al., 1983). If the rigidity of rigor mortis is broken by force it can re-establish itself if the process is still ongoing; the re-establishment begins immediately after being broken, the rigidity is weaker but the maximum extent of it is the same as in controls, as is the course of resolution (Krompecher et al., 2008).

Objective measurement of the force required to break the rigidity of rigor mortis was attempted for many years, the first attempt being made in 1919 by Oppenheim and Wacker, but the difficulty in measuring this force is that the strength of the force varies with the stage of development and resolution of the rigor mortis (Krompecher, 2002). The forces involved are initially small, rising rapidly to a maximum, and then reducing gradually over time until resolution occurs. One measurement at one period of time in the duration of the rigor will not reveal any useful information concerning the estimation of the TSD. Krompecher (1994) carried out experiments on groups of rats killed by a standard method and kept at the same temperature of 24°C post mortem. The same force, insufficient to break the rigor, was applied to a limb at varying intervals after death up to 48   hours. It was found that repeated measurements of the intensity of rigor mortis allowed a more accurate estimation of the TSD than a single measurement and Krompecher suggested certain guidelines: (1) If there was an increase in intensity, the initial measurements were taken no earlier than 5   hours post mortem. (2) If there was a decrease in intensity the initial measurements were taken no earlier than 7   hours post mortem. (3) At 24   hours postmortem resolution was complete and no further change in intensity should occur. A recent study of 79 deceased patients was undertaken in a hospital mortuary where the time of death was known, where they were all transported to the mortuary within 5   hours and kept at a temperature of 20–21°C (Anders et al., 2013). The aims of the study were to determine if re-establishment of rigor mortis took place in loosened joints after more than 8   hours and, if so, could it be determined how many hours postmortem re-establishment of rigor mortis did occur? Deaths occurred from a variety of disease conditions but because of the small numbers, no correction was possible for disease state. Rigor mortis was loosened in 174 joints of 44 deceased persons between 7.5 and 10.5   hours post mortem to determine whether re-establishment occurred after 8   hours and 140 joints were examined after loosening at 15–21   hours post mortem to determine how many hours postmortem re-establishment could occur. The study found that 121 of 314 joints (38.5%) showed re-establishment of rigor mortis between 7.5 and 19   hours and the authors concluded that the currently accepted view that rigor mortis could only be studied to determine the time of death less than 8   hours post mortem, required re-evaluation by further studies. Attempts have been made to standardize the measurement of the force of rigidity in rigor mortis but they have not received widespread acceptance (Schuck et al., 1979; Vain et al., 1992). Because of the subjective nature of the assessment of rigor mortis and the number of variable factors determining its onset, duration, and resolution, it should only be used in conjunction with other methods when estimating TSD (Henssge and Madea, 2002).

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Meat: Conversion of Muscle into Meat

R. Warner , in Encyclopedia of Food and Health, 2016

Process of Rigor Mortis

The process of rigor mortis is one of the recognizable signs of death as a result of the chemical changes in the muscles, causing the musculature to lose extensibility and become stiff. Figure 4 shows the changes that occur postharvest, using a pig carcass as an example. Synthesis of ATP is initially by creatine phosphate (CP) but later by glycogenolysis and glycolysis. CP usually drops to low levels within 1–2   h postharvest. Once CP levels drop to 75% of initial levels, ATP starts to decline. As CP disappears, Pi increases in the cell postharvest, and lactate accumulates concomitantly with increasing hydrogen ion (H+) concentration. Once ATP reaches low levels, the extensibility of the muscles starts to approach 0% of its original, the pH approaches the final pH, and lactic acid reaches its final concentration of 5–6   μmol   g−   1 of tissue (in a well-fed, rested animal). Rigor mortis is defined by the decline of ATP to zero, 0% extensibility, an ultimate pH that is reached, and the production of lactic acid that has plateaued.

Figure 4. Chemical and physical changes in muscle postharvest. The pattern shown is typical for pig muscle undergoing normal postharvest metabolism. Abbreviations: ATP, adenosine triphosphate; CP, creatine phosphate; LA, lactic acid; Ext, extensibility.

 Reproduced from Greaser, M. L. (2001). Postmortem muscle chemistry. In: Hui, Y. H., Nip, W.-K., Rogers, R. W. and Young, O. A. (eds.) Meat science and applications, pp. 21–37. New York: Marcel Dekker.

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CAUSES OF DEATH | Postmortem Changes

M.J. Lynch , in Encyclopedia of Forensic Sciences, 2000

Rigor mortis

The development of postmortem rigor mortis is a predictable postmortem response. Biochemically it represents postmortem muscle contraction which becomes fixed due to the inevitable diminution of available adenosine triphosphate (ATP). It appears first in the smaller central muscle groups such as the jaw and face and moves peripherally. It declines in the reverse order. Some textbooks provide a framework within which to estimate time of death based on development of rigor mortis. However, these are crude estimates and furthermore their use in assisting with determination of time of death is confounded by the notion of 'cadaveric spasm'. This is a phenomenon whereby in an individual engaged in some form of intense physical activity immediately prior to death, the development of rigor can occur as an immediate postmortem response.

The changes which occur in the skeletal muscle postmortem are chemical reactions and as such may be accelerated by an increase in temperature. Thus a body that has been exposed postmortem to high environmental or ambient temperatures may develop rigor at a more rapid rate than expected. Similarly, the death of an individual occurring in a cold environment or refrigeration immediately postmortem will delay the onset of rigor mortis.

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