Rigor mortis, also known as death stiffening or cadaveric rigidity, is a state of stiffening of muscles, sometimes with slight shortening of the fibers. Individual cell death takes place in this stage.
Mechanism of Rigor Mortis
Rigor mortis is a physico-chemical change that occurs within muscles. A voluntary muscle consists of bundles of long fibres. Each fibre is formed of densely packed myofibrils extending through its whole length.
These myofibrils are the contractile elements, and are made up of protein filaments of two types, actin filaments (thin) and myosin filaments (thick) which form a loose physicochemical combination called actomyosin, which is physically shorter than the two substances uncombined.
In the relaxed condition, the actin filaments interdigitate with the myosin filaments only to a small extent. Under the influence of the nerve impulse, the arrays of actin filaments are drawn into the arrays of myosin filaments, rather like pistons into cylinders. This causes the muscle to contract.
During life, the separation of the actin and myosin filaments, and the energy needed for contraction are dependent on adenosine triphosphate (ATP). Three metabolic systems are responsible for maintaining a continuous supply of ATP in the muscle:
(1) Phosphagen system.
(2) Glycogen-lactic acid system.
(3) Aerobic system.
ATP is responsible for elasticity and plasticity of the muscle. The de-phosphorylation of ATP by the action of ATPase produces ADP and phosphate, and a large amount of energy, which is used for muscle contraction. The lost ATP is replaced during life by re-synthesis, which is dependent upon the supply of glycogen. At the time of somatic death, enough ATP is present in the muscle to maintain relaxation.
After death the ATP is progressively and irreversibly destroyed leading to increased accumulation of lactates and phosphates in the muscles. There is no re-synthesis of ATP. The postmortem alteration of ATP is due to dephosphorylation and deamination.
Postmortem loss of integrity of the muscle cell sarcoplasmic reticulum allows calcium ions to flood the contractile units of the muscle fibers (sarcomeres) initiating the binding of actin and myosin molecules and mimicking the normal contraction process.
Normal relaxation in life is achieved by energy-dependent (ATP-driven) pumping of calcium back across the membrane of the sarcoplasmic reticulum, but this fails after death because of membrane disruption and lack of ATP, due to which increased calcium level in the sarcomeres causes muscle contraction.
When the ATP is reduced to a critical level (85% of the normal), the overlapping portions of myosin and actin filaments combine as rigid link of actomyosin, which is viscous and inextensible, and causes hardness and rigidity of muscle rigor.
The rigidity of the muscle is at its maximum, when the level of ATP is reduced to 15%. The actin-myosin complex is trapped in a state of contraction until it is physically disrupted by the onset of putrefaction.
This process is characterized by proteolytic detachment of actin molecules from the ends of the sarcomeres, and consequent loss of the structural integrity of the contractile units. The muscles then soften and relax.
The Order of Appearance of Rigor
All muscles of the body, both voluntary and involuntary are affected. It does not start in all muscles simultaneously (Nysten’s rule). It first appears in involuntary muscles; the myocardium becomes rigid in an hour.
It begins in the eyelids, neck and lower jaw and passes upwards to the muscles of the face, and downwards to the muscles of the chest, upper limbs, abdomen and lower limbs and lastly in the fingers and toes.
Such a sequence is not constant, symmetrical or regular. In individual limbs, it disappears in the same order in which it has appeared. Rigor mortis always sets in, increases and decreases gradually.
Shapiro (1950) suggests that rigor mortis does not follow the anatomical sequence usually described. He suggests that as rigor mortis is a physicochemical process, it is most likely to develop simultaneously in all the muscles, although the changes are more easily first detected in the smaller masses than in the larger.
The proximo-distal progression is more apparent than real, for the sequence is determined by the bulk and kind of muscle involved. This would explain the fixation of elbow or knee joints at an earlier stage than the shoulder or hip joints, but this does not explain why the small muscles of the fingers and toes should be the last to stiffen.
When rigor is fully developed, the entire body is stiff, the muscles shortened, hard and opaque; knees, hips, shoulders and elbows are slightly flexed and fingers and toes often show a marked degree of flexion.
Rigor of erector pilae muscles attached to the hair follicles, may cause roughness, pimpling or goose-flesh appearance of the skin with elevation of the cutaneous hairs, known as cutis anserina or goose skin.
The testes may be drawn up into the groin; semen may be forced out of the seminal vesicles, and the pupils may be partially contracted. Rarely, if the uterus is in labour at the time of death, the rigor mortis may cause the uterus to contract and expel the foetus.
Rigor is tested by trying to lift the eyelids, depressing the jaw, and gently bending the neck and various joints of the body. Note the degree (absent, minimal, moderate, advanced or complete) and distribution.
Development
The development of rigor is concerned with muscles only. It is independent of the integrity of the nervous system, though it is said to develop more slowly in paralysed limbs. Before rigor mortis develops, the body can be moved to any posture, and the rigor will fix in that posture.
When rigor is developing, the extremities can be moved and the rigor, temporarily overcome, develops later and fixes the extremities in their new position, although the rigidity will be less than other symmetrical groups, which have not been disturbed.
If force is applied when rigor is fully developed, stiffness is broken up permanently and the rigid muscles may show postmortem ruptures. Frequent handling of the body breaks the rigor in certain places, leaving a patchy distribution.
Skeletal muscle contains two types of fibres –
Type I (red) which are rich in mitochondria with dominant oxidative metabolism.
Type II (white) which are relatively poor in mitochondria with dominant glycolytic metabolism.
Rigor occurs at different times in the above types of muscles. The fibres which are still slack and some others which are not fully contracted, retain capacity for reversible binding of myosin heads to actin filaments. Re-establishment of rigor occurs due to contraction of such fibres.
P.M. Changes
The contraction of the heart muscle due to rigor mortis should not be mistaken for myocardial hypertrophy. Secondary muscular flaccidity may result in distension of the atria or ventricles, which should not be mistaken for ante- mortem dilatation of the chambers, or myocardial degeneration. Because of these postmortem changes, it is not possible to determine at autopsy whether a heart has stopped in systole or diastole.
Muscle relaxation immediately after death with opening of the eyes and mouth and subsequent fixation in rigor morris often occur after death, giving the face the appearance of grimacing, but this does not reflect whether the individual’s last moments were of fear or fright.
Time of Onset
It begins one to two hours after death and takes further one to two hours to develop. In temperate countries, it begins in three to six hours and takes further two to three hours to develop.
Duration of Rigor Mortis
Usually it lasts 24 to 48 hours in winter and 18 to 36 hours in summer. It lasts for 2 to 3 days in temperate regions. These times are variable, because of many extrinsic and intrinsic factors. ‘When rigor sets in early, it passes off quickly and vice versa.
Conditions Altering the Onset and Duration:
(1) AGE : Rigor does not occur in a foetus of less than seven months, but is commonly found in stillborn infants at full term. In healthy adults, it develops slowly but is well-marked and lasts longer, while in children and old people it is feeble and rapid.
(2) NATURE OF DEATH : The onset of rigor is early and duration is short in deaths from diseases causing great exhaustion and wasting, e.g., cholera, typhoid, tuberculosis, cancer, etc. and in violent death as by cut-throat, firearms, electrocution, lightning and in strychnine poisoning. In organophosphate poisoning rigidity appears early. CO poisoning delays disappearance. The onset is delayed in deaths from asphyxia, severe haemorrhage, apoplexy, pneumonia, and nervous disease causing paralysis of muscle. It may disappear very rapidly in case of widespread bacterial infection, especially in gas gangrene, where putrefaction begins early. Rigor mortis is frequently absent in persons dying from septicaemia.
(3) MUSCULAR STATE : The onset is slow and the duration long in case where muscles are healthy and at rest before death. The onset is rapid, and duration short, if there is fatigue or exhaustion (violent or heavy exercise, severe convulsions) before death. In persons who run prior to death, rigor may develop earlier and rapidly in their legs, compared to other parts. Rigor may be delayed or very weak in emaciated persons.
(4) ATMOSPHERIC CONDITIONS : The onset is slow and duration long in cold weather. Rigor persists longer in cold wet air than in fresh dry air. It is prolonged by dry cold air and cold water. The onset is rapid due to heat, because of the increased breakdown of ATP but the duration is short. If the body is in an extremely hot environment and decomposition begins, rigor mortis may disappear in 12 hours after death. It may persist for 3 to 4 days in refrigerated conditions.
Because of the number and variability of the factors which influence the development of rigor mortis, it is not possible to draw any general rule for the rate of its onset, duration and disappearance.
Medicolegal Importance
(1) It is a sign of death.
(2) Its extent helps in estimating the time of death, which is not reliable.
(3) It indicates the position of the body at the time of death.
If the body is lying on its back with its lower limbs raised in the air, it indicates that the body reached full rigidity elsewhere while lying in a position where the legs were flexed or the feet suspended and was later moved to the latter position where the support is no longer present.
Conditions Simulating Rigor Mortis
(1) Heat Stiffening : When a body is exposed to temperatures above 65°C. a rigidity is produced, which is much more marked than that found in rigor mortis. The degree and depth of the change depends on the intensity of the heat and the time for which it was applied. It is seen in deaths from burning, high voltage electric shock and from falling into hot liquid. Heat causes stiffening of the muscles, because the tissue proteins are denatured and coagulated as in cooking.
The muscles are contracted, dessicated or even carbonised on the surface. A zone of brownish-pink ‘cooked meat’, is seen under this, overlying normal red muscle. Changes in posture, especially flexion of the limbs occur due to muscle contraction. The stiffening remains until the muscles and ligaments soften from decomposition and the normal rigor mortis does not occur.
(2) Cold Stiffening : When a body is exposed to freezing temperatures, the tissues become frozen and stiff, due to freezing of the body fluids and solidification of subcutaneous fat simulating rigor. The body is extremely cold and markedly rigid. When the joints are forcibly flexed, crackling of the ice occurs in the synovial fluid. If the body is placed in warm atmosphere, the stiffness disappears and after a time, the normal rigor mortis occurs rapidly and passes off quickly. Hardening of the subcutaneous fat especially in infants sometimes makes the skin-folds rigid, which may be mistaken for ligature mark.
(3) CADAVERIC SPASM or Instantaneous Rigor: Cadaveric spasm (cataleptic rigidity) is a rare condition. In this, the muscles that were contracted during life become stiff and rigid immediately after death without passing into the stage of primary relaxation.
As such, the change preserves the exact attitude of the person at the time of death for several hours afterwards. It occurs especially in cases of sudden death, excitement, fear, severe pain, exhaustion, cerebral haemorrhage, injury to the nervous system, firearm wound of the head, convulsant poisons, such as strychnine, etc.
The spasm is primarily vital phenomenon, in that it originates by normal nervous stimulation of the muscles. This is usually limited to a single group of voluntary muscles and frequently involves the hands. Occasionally, the whole body is affected as seen in soldiers shot in battle, when the body may retain the posture which it assumed at the moment of death.
No other condition simulates cadaveric spasm and it cannot be produced by any method after death. Very great force is required to overcome stiffness. It passes without interruption into normal rigor mortis and disappears when rigor disappears. Coagulation of protein is seen in burns on microscopic examination but not in cadaveric spasm.
