CHANGES IN MUSCLE

Death and Changes after Death

After death, three sort of changes are identiﬁ ed in the muscles and these changes are as follows (Fig. 7.17):

1. Primary relaxation or primary ﬂ accidity of muscles 2. Rigor mortis

3. Secondary relaxation or secondary ﬂ accidity of muscles Primary Relaxation

• This state of muscle begins with somatic death and in this phase molecular death does not occur.

• This stage lasts for 1-2 hours.

• All the muscles, voluntary and involuntary, are relaxed after death.

• Since the molecular death has not occurred, the muscles may respond to mechanical, electrical or chemical stimuli.

In a recent study, muscular response to electrical stimulation had been elicited up to 8th hour after death.²⁵ Mechanical excitability of skeletal muscles can be identiﬁ ed up to 1.5

to 2.5 hours after death. If the quadriceps femoris muscle is stroked with hammer about 10 cm above the patella will cause upward movement of limb because of contraction of muscle. This sort of mechanical excitability is called as tendon reaction or Zasko’s phenomenon. Peristalsis may occur in intestine with cilia movement of intestinal cells.

Pupils react to atropine or physostigmine.

• In this stage, the muscle reaction is alkaline and the anaerobic activity in cells may continue.

Rigor Mortis

Synonyms: Cadaveric rigidity (rigor = rigidity, mortis = of death)

Deﬁ nition

Rigor mortis is that state of muscles of dead body where they become stiff with some degree of shortening that follows the period of primary ﬂ accidity.

Rigor mortis is the stiffening of muscle after death. Along with stiffening of muscle, shortening of muscle ﬁ bers, albeit small, have been noted. When rigor mortis is developed completely, the body and joints become stiff with ﬂ exion attitude of upper limb muscles (Fig. 7.18). Appearance of rigor mortis indicates death of individual cells (i.e. molecular death has occurred).

Forensic Anatomy and Physiology of Muscle Before proceeding to mechanism, it is worth revising basic feature of muscle and its physiology. Skeletal muscle is com-posed of individual muscle fi bers and each muscle fi ber is a single cell that is multinucleated. The muscle fi ber is long, cylindrical and is surrounded by sarcolemma. The muscle fi bers are made up of myofi brils. Each myofi bril is composed Table 7.10: Color of lividity and cause of death

Cause Colour Mechanism

Carbon monoxide Pink Carboxyhemoglobin

Cyanide Cherry-red Excessive oxygenated blood

Fluoroacetate Pink/cherry red Excessive oxygenated blood

Refrigeration Pinkish Retention of oxygen in Cutaneous blood by cold

Hypothermia Pinkish Retention of oxygen in Cutaneous blood by cold

Sodium chlorate Brown Methemoglobin

Hydrogen sulﬁ de Green Sulfhemoglobin

Aniline Deep blue Deoxygenated blood

Carbon dioxide Bluish Deoxygenated

FIG. 7.17: Changes in muscles after death

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of fi laments. The fi laments are of two types, the thinner one is called as actin and the thicker one is called as myosin. Each myofi bril is surrounded by sarcoplasmic reticulum. The con-tractile mechanism in skeletal muscle depends on:

1. Myosin 2. Actin 3. Tropomyosin

4. Troponin – troponin I, troponin T, troponin C.

Sequence of Contraction and Relaxation in Life²⁶

• For contraction – discharge of motor neuron → release of acetylcholine at motor end plate → binding of ace-tylcholine to receptor → Increased sodium and potas-sium conductance in end-plate membrane → generation of end-plate potential → generation of action potential in muscle ﬁ bers with inward spread of depolarization along T tubules → release of calcium from sarcoplasmic reticulum → calcium bind with troponin C and un-cov-ers binding site on actin → formation of cross-linkages between actin and myosin and sliding of actin ﬁ laments over myosin causing shorting and thus contraction (Fig. 7.19 A).

• For relaxation – calcium pumped back into sarcoplas-mic reticulum → release of calcium from troponin C

→ cessation of interaction between actin and myosin → relaxation of muscles (Fig. 7.19 B).

• Note that ATP provides the energy for both contraction and relaxation.

Mechanism of Rigor Mortis

• In life, for contraction and relaxation of muscles, ATP is required.²⁶ Thus the process is ATP dependent. The

ATP is in high contraction in resting muscle and the balance between ATP consumption and re-synthesis is maintained. For synthesis of ATP, glycogen is required.

After death, the failure of re-synthesis of ATP leads to a fall in its concentration within the muscle and accounts for the hardness and rigidity of muscle – the rigor mortis (stiffness after death).

• The extensibility of muscle begin to fall when its ATP levels drops to 95% and the muscles are least extensible when the ATP falls to the level of 15% of normal.

• At the time of somatic death, enough ATP is present in muscle to maintain the process of relaxation. For this process constantly ATP is breakdown to ADP and phosphate. For some time after somatic death, so long glycogen is available in the muscle, there is re-synthe-sis of ATP. With depletion of glycogen amidst anaero-bic respiration and constant accumulation of lactate and phosphate in the muscle, no further ATP re-synthesis is possible and muscle begins to lose softness, elasticity and FIG. 7.18: Appearance of rigor mortis in body. Note

the joints become stiff and the entire body can be placed over small top of table with maintaining the posture of trunk and lower limbs

FIGS 7.19A to C: Diagram showing muscle during life and changes occurring after death

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extensibility. Thus, gradually there is formation of viscid gel like acto-myosin complex that leads to stiffening and some shortening of muscles (Fig. 7.19 C).²⁷

• The muscles remain in rigor until the muscle proteins are destroyed. The destruction of muscles is brought by autolysis caused due to release of enzyme lysosomes and heralds onset of decomposition.

Onset and Disappearance of Rigor Mortis

• Rigor mortis occurs in all sort of muscles i.e. striated, smooth and cardiac muscles

• It occurs earlier in involuntary muscle than voluntary muscle.

• In summer season, rigor mortis fi rst appear in heart mus-cle at the end of fi rst hour after death. In case of volun-tary muscle, rigor mortis fi rst appears in muscle of eye lids (orbicularis occuli).

• Rigidity spreads gradually within next few hours, chronologically, in the muscles of face, neck, jaw, trunk, upper limbs (from shoulder to hand), and lower limbs (from hip to foot). It appears lastly in the small muscles of hand and feet (Fig. 7.20). It disappears in the same fashion as followed in onset i.e. it disappears ﬁ rst in the muscles of face, neck, jaw, trunk, upper limbs (from shoulder to hand), and lower limbs (from hip to foot). It disappears lastly in the small muscles of hand and feet.²⁸

• Rule of 12: It is generally considered that it takes about 12 hours after death to develop rigor mortis, remains for another 12 hours and takes about 12 hours

to pass-off. This is also called as March of rigor (Fig.

7.21). This is only generalized categorization and the appearance and disappearance depends on number of factors. In India, even different states show consider-able difference.

• The appearance and disappearance of rigor mortis as noted in the recent study conducted in India²⁸ is pre-sented in Table 7.11.

Rigor in Internal Organs and Pupils

• Rigor may affect the pupil rendering them in unequal size.

• In heart, rigor causes ventricles to contract and may be mistaken for ventricular hypertrophy

• Rigor may affect dartos muscle of scrotum that com-presses the testes and epididymis – causes postmortem emission of semen.²⁹

FIG. 7.20: Appearance of rigor mortis

Table 7.11: Stay of rigor mortis in India Months Stay of rigor mortis

April to June 11 hours 25 minutes to 28 hours 25 minutes

July to September 17 hours 15 minutes to 34 hours 20 minutes

October to December 16 hours 25 minutes to 61 hours 5 minutes

January to March 19 hours 5 minutes to 50 hours 15 minutes

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Factors

Appearance of rigor mortis depends on many factors such as:

1. Age – it does not occur in fetus less than 7 months of intrauterine life, however, a case was reported in Modi’s Textbook of Medical Jurisprudence that rigor mortis was recorded in 5 month fetus at Bombay famine hospital.

2. Physique of the person – rigor mortis appear early and passes off early in thin built subjects with weak muscu-lature in comparison with well-built people.

3. Season – in summer season with high atmospheric tem-perature, rigor mortis appear early and passes off early in comparison with winter season with low environmental temperature.

4. Cause of death – rigor may appear early and passes off early in deaths preceded by high muscular activity caus-ing considerable depletion of glycogen storage in mus-cle whereas in certain conditions the onset is delayed.

In certain deaths, it appears early but stays longer. The conditions are presented in Table 7.12.

5. Condition of muscles before death – if the muscles are relaxed, then rigor sets late. If the muscles are exhausted then rigor mortis set early and passes-off early.

Medicolegal Importance

1. Presence of rigor mortis is sign of death 2. Time since death can be estimated 3. Indicates position of the body

4. Rigor mortis may be confused with cadaveric spasm, heat stiffening, cold stiffening

5. Breaking of rigor mortis – due to handling of the body or when force is used, the stiff joints may get loosened with breaking of rigor mortis. When breaking of rigor

mortis occur in this fashion then the muscles do not resume rigor again. Such picture may cause difﬁ culty in estimating time since death.

6. Rigor mortis is not functionally related with the nervous system, and therefore it is also developed in paralyzed limb.³¹

Differential Diagnosis Rigor mortis may be confused with 1. Cadaveric spasm

2. Heat stiffening 3. Cold stiffening 4. Gas stiffening Cadaveric Spasm

Synonyms: Instantaneous rigor, instant rigor, cataleptic rigidity

• This is a rare condition

• Cadaveric spasm is a state where muscles or group of muscle, instead of going under primary relaxation after death, go into a sudden state of stiffening.

• The cause of this sudden stiffening is not known but is usually associated with violent deaths coupled with emotional disturbances at the time of death.

• Usually after death, the muscles undergo primary stage of relaxation. However, in certain deaths with cadav-eric spasm, the muscles do not undergo primary stage of relaxation, rather they get stiffened at the moment of death.

• For example – in case of drowning deaths, the weeds/

grass/mud/sand may be tightly grasped in hand or in case of suicide by shooting with ﬁ rearm, the weapon may be ﬁ rmly grasped in the hand.

• Cadaveric spasm continues through the stage of rigor mortis of the body and disappears with the onset of sec-ondary relaxation.

• The condition commonly involves only a group of FIG. 7.21: March of rigor

Table 7.12: Onset of rigor mortis and the conditions

Rigor mortis Cause Early onset and

passes of early

Electrocution,³⁰ cancer, convulsions, hyperpyrexia, metabolic acidosis, uremia, hot environmental conditions Delayed onset Asphyxia, apoplexy, cold

environ-mental conditions, hypothermia Rapid onset but

stays longer Strychnine, hydrocyanic acid poisoning

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muscles of hand or limb but rarely whole body may be involved.

• Differences between rigor mortis and cadaveric spasm are given in Table 7.13.

Medicolegal Importance

1. Presence of cadaveric spasm indicate that person was alive at the time of instantaneous rigor

2. If weeds/mud/grass particles are found grasped in hand in a drowned body, it indicates antemortem nature of drowning.

3. Presence of some object (like knife) or foreign body (like button, torn cloth, hairs etc.) may helpful in investigation to relate these things with crime.

Heat Stiffening

• When body is subjected to temperature above 65^oC, rigid-ity develops in the body. This rigidrigid-ity is due to coagula-tion of muscle proteins causing contraccoagula-tion of muscles.

• Such heat stiffening is associated with burns or high volt-age electric burns.

• The stiffening remains until the muscles and ligaments get soften due to decomposition and in such state, the rigor mortis do not occur.

• Differences between rigor mortis and heat stiffening are given in Table 7.14.

Cold Stiffening

• When the body is subjected to freezing temperature, the tissue becomes frozen and gets stiff. Freezing causes solidiﬁ cation of body ﬂ uids and fat. Such cold stiffen-ing simulates rigor mortis.

• If such body is re-warmed then the stiffness disappears and after that the rigor mortis sets in.

Gas Stiffening

• This sort of stiffening occurs in dead bodies showing signs of decomposition

• Due to decomposition, false rigidity is produced in the body due to accumulation of gases in the tissues.

Secondary Relaxation of Muscles

• It consists of secondary relaxation of muscles following rigor mortis and the changes are brought by the action of alkaline medium produced by putrefaction.

• Here the muscles become soft and ﬂ accid. The muscle reaction is alkaline.

• No response to mechanical, electrical or chemical stimuli occur.

• Differences between primary relaxation and secondary relaxation of muscle are presented in Table 7.15.

DECOMPOSITION

Deﬁ nition

It is disintegration of body tissues after death.

Decomposition is normal fate of an indisposed body. How-ever, under certain specifi c environmental conditions, modi-fi ed decomposition of the dead body occurs and in such cases instead of early and total destruction of dead body, it is pre-served for considerable time. Such modifi ed decomposition may occur in form of mummifi cation or adipocere formation (Fig. 7.22).

Categories and stages of decomposition³² 1. Early decomposition

2. Advanced decomposition 3. Partial skeletonization 4. Skeletonization

Table 7.13: Difference between rigor mortis and cadaveric spasm

Features Rigor mortis Cadaveric spasm

Time of onset 1-2 hours after death Immediate

Muscles involved All muscles of body are involved gradually Usually group of muscles (like hand) are involved

Degree of stiffness Comparatively moderate Comparatively strong

Predisposing factors None Excitement, fear, emotional disturbance,

etc.

Mechanism Break down of ATP Not known

Medicolegal importance Helps to know time since death, position

of body. Help to suggest manner of death

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Mechanism

Decomposition follows the arrest of biochemical process that develops, maintains and preserves the integrity of cellular ele-ment. During decomposition, the tissue components leak and break up releasing hydrolytic enzymes. The complex organic body tissues are break down into simpler compounds. The bacteria and other microorganism thrive on the unprotected organic components of the body. Thus, two parallel process of decomposition can be identiﬁ ed as follows (see Fig. 7.22).

It should be noted that these process proceed simultaneously and for convenience it has been described separately.

1. Autolysis – Self dissolution of body tissues by the enzymes released from the disintegrating cells.

2. Putrefaction – These are the changes produced by the action of bacteria and other microorganism thriving on the body.

3. A third kind of postmortem destruction can be identiﬁ ed in some bodies that are not disposed. Such postmortem destruction is brought out due to attack of various types of animals such as insect, rodents, canines, fox, jackal, vulture, ﬁ sh etc.

Autolytic Changes

• Autolysis is a process of self-destruction of body tissues by enzymes. The process may also occur in living per-son characterized by focal tissue injury and necrosis sur-rounded by inﬂ ammatory reaction. The same mechanism operates after death, however, in dead body, the process occurs on large scale and devoid of vital (inﬂ ammatory) reaction (as the living property is no more!). Autolysis is

thought to be stimulated by the decrease in intracellular pH due to decreased oxygen level followed after death.

• This process occurs earlier and rapid in some tissues rich in hydrolytic enzymes such as pancreas and gastric mucosa;

intermediate in tissues like heart, liver and kidneys and delayed in ﬁ brous tissue like uterus or skeletal muscle.

• The process of autolysis is temperature dependent.

Refrigeration of a body soon after death will retards the enzymatic self-digestion of cells whereas increase in tem-perature promotes degradation as seen in deaths preceded by fever, exertion or death in high ambient temperature.

• The phenomenon of autolysis is visible on gross and microscopic examination. For example grossly autoly-sis is observed as a skin slippage. In skin slippage, the release of hydrolytic enzymes releasing at dermo-epi-dermal junction causes loosening of epidermis from the underlying dermis as a result, the epidermis is easily peel-off the dermis (Fig. 7.23). Similarly hairs and nails are loosened. Microscopically, autolysis is identiﬁ ed by homogenous and eosinophilic cytoplasm with loss of cel-lular details with cell remains as debris.

• Internally autolysis can be noticed as a doughy consist-ency of the organs. Similarly the intima of large blood vessels appears stained by postmortem hemolysis. This hemolysis is nothing but autolysis of red blood cells.

• Gastromalacia is postmortem rupture of gastric wall due to the process of autolysis. It usually occurs in fun-dus area and is devoid of any vital reaction. Similarly oesophagomalacia is postmortem rupture of lower end of oesophagus due to autolysis and lacks vital reaction.

Table 7.14: Difference between rigor mortis and heat stiffening

Features Rigor mortis Heat stiffening

Nature Postmortem May be antemortem or postmortem

Degree of stiffness Comparatively moderate Comparatively high

Mechanism Break down of ATP Due to coagulation of muscle

Associated features Nothing speciﬁ c Signs of exposure to heat will be present for example burning, blisters, heat rupture etc

Table 7.15: Difference between primary and secondary relaxation of muscles Features Primary relaxation Secondary relaxation

Time of onset Immediately after death After disappearance of rigor mortis and when decomposition occurs

Molecular death No Yes

Response to stimuli (Mechanical and electrical)

Present Absent

Associated features Nothing particular Signs of decomposition present

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• Disintegration of dead fetus in mother’s womb is called as maceration and it is considered as aseptic autolysis.

Putrefaction

• Putrefaction changes depend on various factors as described below. Microorganisms responsible are – Clostridium welchii, B. coli, Staphylococci, non-hemo-lytic Streptococci, Dyptheroids, Proteous etc.

• As the process of putrefaction progresses, different gases are produced such as – hydrogen sulphide, carbon dioxide, mercaptans, methane, ammonia, etc. Methane burns read-ily when ignited. The rapid production and accumulation

of gases causes both physical and chemical changes in the decomposing body as mentioned in Table 7.16.

• The physical changes consist of bloating the features with distension of abdomen by distending gases (Fig.

7.24). This causes obliteration of the identity of the deceased. In males, the gas is forced from the peritoneal cavity down the inguinal canal into the scrotum causing scrotal swelling.

• Different gases of decomposition induce the chemical changes. For example the hydrogen sulﬁ de readily diffuses through the tissues. It reacts with hemoglobin to form sulf-hemoglobin. This pigment initially outlines the superﬁ cial blood vessels and as decomposition progresses, a general-ized green hue may be imparted to body (Fig. 7.25).

• Putrefaction occurs at different rate in various body tis-sues and depends up on their moisture content. Three main changes are noticed during putrefaction as:³³ FIG. 7.22: Showing late changes after death

FIG. 7.23: Peeling of skin

Table 7.16: Importance of gases of decomposition - Causes bloating of features causing difﬁ culty in identi-ﬁ cation

- Causes disintegrating and shifting of postmortem lividity causing difﬁ culty in assessing the position of body - Causes postmortem purging of feces, semen, decom-position ﬂ uid

- Causes expulsion of fetus from uterus

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1. Change in color 2. Liberation of gases

In document [Rajesh Bardale] Principles of Forensic Medicine and Toxicology (Page 166-181)