Changes in the skin:

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• Changes in the skin
• Within a few minutes after death, the skin
  becomes pale ashy-white and loses elasticity.
  The lips appear brownish, dry and hard due to
  drying.
• Changes in the eye
• (1) Loss of corneal reflex Found in all cases
  of deep insensibility, so not a reliable sign of
  death.
• (2) Opacity of the cornea May occur in cholera
  and wasting diseases before death. due to
  drying and is delayed if lids are closed after
  death. If eyelids are open for a few hrs after
  death, a film of cell debris and mucus from brown
  triangles on the sclera at each side of the iris
  called tache noir within a few hrs, upon which
  dust settles and the surface becomes wrinkled.
• (3) Flaccidity of eyeball Due to redn in I.O.Pr
  eyes look sunken and softer. Soon after death
  I.O.Pr is lt12gm within half an hr lt3gm and
  becomes nill at the end of 2 hrs.
• (4) Pupils Soon after death, pupils are
  dilated, bcoz of relaxation of muscles of iris.
  Later, constricted with onset of rigor mortis of
  constrictor muscles evaporation of fluid. The
  pupils react to atropine and eserine for about 1
  hr after death, but do not react to strong light.
  Shape of pupil not changed by pressure during
  life, after death if pressure applied on eyeball,
  the pupil becomes oval, triangular or polygonal.
• (5) Retinal vessels Fragmentation or
  segmentation of blood columns soon. Retina is
  pale for 2 hrs. At 6 hr, the disk outline is
  hazy, blurred in 7 to 10 hrs.
• (6) Chemical changes Rise if K values in
  vitreous humour after death.

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Tache noir
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• COOLING OF THE BODY (Chill of death, algor
  mortis)
• The body cools rapidly on the surface and more
  slowly in the interior.
• The body heat is lost by conduction, convection
  and radiation. The curve of cooling is sigmoid in
  pattern, bcoz of some residual enzymatic activity
  and due to retention of heat for sometime.
• In serious illness, O n begins to fail before
  death, and hands feet become cooler than the
  rest of the body gradual cooling of the trunk.
• In sudden death, the cooling starts after death.
• The rectum is the ideal place to record
  temperature except in cases of sodomy. The
  thermometer should be inserted 8 to 10 cm and
  left there for 2 minutes. The time of this
  reading is recorded and temperature of
  environment is recorded at the same time.
• A rough idea of approximate time in hours of
  death can be obtained by using the formula
  Normal body temp - rectal temp / Rate of temp
  fall per hour.
• In many cases of asphyxia, fat or air embolism,
  certain infections, heatstroke and in pontine
  hge, drug reactions, etc a sharp rise of temp
  occurs. Exercise or struggle prior to death may
  rise rectal temp up to 1.5 to 2 deg C.
• Low temp occurs in cases of collapse, CCF,
  massive hge, etc.
• During sleep, the rectal temp is 0.5 to 1 deg C
  lower.

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• Factors affecting rate of cooling
• The difference in temp b/w the body medium If
  the difference is great, the fall of temp is
  rapid. During summer, the environment temp is
  higher than body temp, so cooling is very slow.
• The built of the cadaver Rate of heat loss ? to
  surface area. So, children and old people cool
  more rapidly than adults.
• The physique of the cadaver Fat bodies cool
  slowly than lean bodies.
• The environment of the body In a well-ventilated
  room, body will cool more rapidly than in a
  closed room. A body immersed in cold water cools
  rapidly the rate of fall being almost twice as
  fast as by air cooling. Bodies buried in earth
  cool rapidly than those in air, but more slowly
  than those in water.
• Covering on or around the body Slow when body is
  clothed.
• The rectal temp of an average-sized naked body
  reaches that of environment in 20 hours. A body
  in zero weather may undergo freezing and become
  stony-hard from formation of ice in cavities and
  blood vessels. The ice inside the skull may
  expand and cause separation of sutures.
• MLI Helps in estimation of the time of death.
• Postmortem Caloricity Here, the temp of body
  remains raised for the first 2 hrs or so after
  death. This occurs (1) when reguln of heat prod
  is disturbed before death, in sunstroke. (2)
  great ?in heat prod in muscles due to convul,
  e.g., tetanus N.Vom poisoning, (3) when
  excessive bacterial activity, septicemia, cholera
  other fevers.

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• POST-MORTEM HYPOSTASIS (Postmortem staining,
  sub-cutaneous hypostasis, livor mortis, cadaveric
  lividity, suggilations, vibices and darkening of
  death)
• It is the bluish-purple or purplish-red discol
  which appears under skin (rete mucosum) of the
  dependent parts of the body after death, due to
  capillo-venous distension. The intensity of the
  colour depends upon the amount of reduced Hb.
• It is caused by stoppage of circulation, stagn of
  blood in vessels its tendency to sink by force
  of gravity.
• It is not possible to distinguish the postmortem
  discol from that prod by cyanosis in the living.
  So, it is not advisable to use cyanosis to
  describe post-mortem appearances.
• It begins as a patchy mottling of the skin. The
  areas then enlarge and fuse to produce extensive
  discoloration. PM lividity begins shortly after
  death, but it may not be visible for about ½ - 1
  hr after death in normal individuals, from
  about 1- 4 hrs in anaemic persons.
• It is usually well-dev within 4 hrs and reaches a
  maximum b/w 6 12 hrs. it is present in all
  bodies, but more clearly in fair people than in
  dark.
• The extent time of app of lividity mainly dep
  upon
• The vol of blood in circulation at the time of
  death.
• The length of time that the blood remains fluid
  after death.
• Hypostatic congestion PM hypostasis seen a few
  hrs after death in case of a person dying slowly
  with circulatory failure, e.g., cholera, typhus,
  Tb, uraemia, CCF asphyxia. Here, hypostasis
  will be marked shortly after death.

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• It is intense in asphyxia, where the blood may
  not readily coagulate, is less marked in death
  from hge, anaemia wasting ds due to reduced
  amount of blood and pigment. Less marked in lobar
  pneumonia, and other conditions where blood
  coagulates quickly.
• The distribution of the stain depends on the
  position of the body.
• In a body lying on its back, it 1st appears in
  the neck, then spreads over the entire back
  with the exception of the parts directly pressed
  on.
• Any pressure prev the capillaries from filling,
  such as the collar band, waist band, belts,
  wrinkles in the clothes, etc and such areas
  remain free from colour and are seen as strips
  and bands called vibices.
• The location of the lividity indicates the
  position of the body during PM interval.
• If body has been lying on one side, the blood
  will settle on that side, and if lying on back
  the staining will be seen on the back.
• If the body has been suspended in the vertical
  position as in hanging, PM hypostasis will be
  more marked on the upper surface of the limbs. In
  drowning, it is usually found on the face, upper
  part of chest, hands, lower arms, feet and the
  claves, as they are the dependent parts.
• If the body is constantly moving its position, as
  after drowning in moving water, the staining may
  not develop.
• When coagulation in capillaries takes place, the
  stains become permanent and this is known as
  fixation of PM staining. This usually occurs in
  about 6 hrs.
• Petechiae or large hges palpable blood
  blisters may dev in areas of hypostasis commonly
  in back of shoulders and neck, sometimes on
  front of chest.

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• The hypostatic areas have distinct colour in
  certain cases of poisoning.
• In CO poisoning, cherry-red
• In HCN poisoning, bright-red
• In poisoning by nitrates, K.chlorate,
  K.bicarbonate, nitrobenzene and aniline (causing
  methaemoglobinemia) red-brown or brown
• Phos poisoning, dark brown.
• In asphyxia, deep bluish-white or purple.
• In exposure to cold and refrigerated bodies, the
  colour is pink, as the wet skin allows the
  atmospheric O2 to pass through, and also at low
  temp, Hb has a greater affinity for O2.
• In septic abortion caused by Cl. welchii, the
  colour is often greyish-brown.
• Hypostasis also occurs in internal organs and the
  dependent parts of the liver, spleen, kidneys,
  larynx, lungs, heart and brain show colour
  changes similar to that in the skin.
• Changes in PM lividity occurs when putrefaction
  sets in. in early stages, there is hemolysis of
  blood diffusion of blood pigment into
  surrounding tissues. As decomposition progresses,
  the lividity becomes dusky in colour turns
  brown and green before finally disappearing with
  destruction of the blood.
• MLI (1) It is a sign of death (2) Its extent
  helps in estimating time of death (3) It
  indicates the position of the body at the time of
  death (4) It may indicate the moving of the body
  to another position sometime after death (5)
  Sometimes, the colour may indicate the cause of
  death.

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• MUSCULAR CHANGES
• After death, the muscles of the body pass through
  three stages
• Primary relaxation or flaccidity
• Rigor mortis or cadaveric rigidity
• Secondary flaccidity.
• Primary flaccidity During this stage, death is
  only somatic it lasts for 1- 2 hrs. All muscles
  of the body begin to relax soon after death. The
  lower jaw falls, eyelids looses tension, and
  joints are flexible. Body flattens over contact
  areas. Peristalsis may occur in bowel, and
  ciliary mvmt mvmt of white cells may continue.
  Pupils react to atropine or physostigmine.
• Rigor mortis is a state of stiffening of
  muscles, sometimes with slight shortening of the
  fibres. Individual cell death occurs at this
  stage.
• Mech During life, the seperation of actin
  myosin fil, the energy needed for contr are dep
  on ATP. ATP is resp for elasticity and plasticity
  of muscle. After death the ATP is progressively
  and irrev destroyed leading to ?accuml of
  lactates and phosphates in the muscles. When the
  ATP is reduced to a critical level (85 of
  normal) the overlapping portions of myosin and
  actin fil combine as a rigid link of actomyosin,
  which is viscous inextensible, and causes
  hardness and rigidity of muscle rigor. Rigidity
  is max at 15. Rigor persists until putrefaction
  sets in. The muscles then soften relax.

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• Order of app of RM All muscles of body, both vol
  invol are affected. It 1st app in invol
  muscles, the myocardium becomes rigid in an hr.
  It begins in the eyelids, neck and lower jaw
  passes upwards to the muscles of face,
  downwards to the muscles of the chest, upper
  limbs, abdomen and lower limbs. RM always sets
  in, increases and decreases gradually.
• The proximo-distal progression of RM is more
  apparent than real, for the sequence is
  determined by the bulk and kind of muscle
  involved.
• When RM is fully developed, the entire body is
  stiff, the muscles shortened, hard and opaque
  knee, hips, shoulders and elbows are slightly
  flexed and fingers and toes often showed marked
  degree of flexion. Rigor of erector pilae muscles
  is known as cutis anserina or goose skin.
• Rigor is tested by trying to lift the eyelids,
  depressing the jaw, and gently bending the neck
  and various joints of the body.
• The dev of RM is concerned with muscles only. It
  is indep of the integrity of nervous system,
  though RM is said to dev more slowly in paralyzed
  muscles.
• Time of onset In India, it begins in 1-2 hrs
  after death and takes further 1-2 hrs to develop.
  
• Duration of RM In India, usually it lasts for
  24-48 hrs in winter and 18-36 hrs in summer. When
  rigor sets in early, it passes off quickly and
  vice versa.
• Conditions altering the onset and duration
• (1) Age, (2) Nature of death, (3) Muscular state
  (4) Atmospheric conditions.

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• Age RM does not occur in a fetus of lt7 months,
  but commonly found in stillborn infants at full
  term. In healthy adults, onset is slow but well
  marked, while in children and old people, it is
  feeble and rapid.
• Nature of death
• In deaths from exhausting or wasting ds e.g.,
  cholera, typhoid, Tb, cancer, etc and in violent
  deaths as by cut-throat, firearms or by
  electrocution, the onset is early and duration is
  short.
• In strychnine or other spinal poisons, the onset
  is rapid and duration is longer.
• In deaths from asphyxia, severe hge, apoplexy,
  pneumonia, nervous ds causing paralysis of
  muscle, and perfusion with normal saline, the
  onset is delayed.
• It may disappear rapidly in case of widespread
  bacterial inf, esp in gas gangrene, where
  putrefaction begins early.
• Muscular state onset is slow, long duration
  healthy muscles, fatigue or exhaustion before
  death hastens its onset. After insulin inj RM dev
  quickly, as the muscle glycogen is reduced.
• Atmospheric conditions onset is slow and
  duration long in cold weather. In hot weather,
  the onset is rapid but duration is short. It may
  persist for 3 to 4 days in refrigerated
  conditions.
• MLI (1) It is a sign of sure death (2) Its
  extent helps in estimating the time of death (3)
  It indicates the position of body at the time of
  death.
• Conditions simulating rigor mortis
• (1) Heat stiffening (2) Cold stiffening (3)
  Cadaveric spasm or Instantaneous rigor

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• Heat stiffening This occurs when the body is
  exposed to temp above 65 degree C. it is seen in
  deaths from burning, high voltage electric shocks
  and from falling into hot liquid. Heat causes
  stiffening of the muscles, bcoz the tissue
  proteins are denatured coagulated as in
  cooking. Changes in posture, esp flexion of the
  limbs occurs due to muscle contraction. It
  remains until the muscles and ligaments soften
  from decomposition and the normal RM does not
  occur.
• Cold stiffening This occurs when body is exposed
  to freezing temp. If the body is placed in warm
  atmosphere, the stiffness disappears and after a
  time, the normal RM occurs.
• Cadaveric spasm or Instantaneous spasm Here, the
  muscles that were contracted during life become
  stiff and rigid immediately after death without
  passing into the stage of primary relaxation. It
  occurs esp in cases of sudden death, excitement,
  fear, severe pain, exhaustion, sudden asphyxial
  death, cerebral hge, injury to nervous system,
  firearm wound of the head, etc. Usually limited
  to small muscle groups and freq involves the
  hands. No other condition simulates CS and it
  cannot be produced by any method after death. It
  passes without interruption into normal RM and
  disappears when rigor disappears.
• This condition is of great medico-legal
  importance.
• Secondary relaxation Muscles become soft and
  flaccid due to breaking down of actomyosin due
  to putrefaction. The reaction of muscle juice
  again becomes alkaline.

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• PUTREFACTION or decomposition is the final stage
  following death, produced mainly by the action of
  bacterial enzymes, mostly anaerobic organisms
  derived from the bowel. The chief destructive
  bacterial agent is Cl.welchii. The other org
  include Streptococci, Staphylococci, B. Proteus,
  B.Coli, B.aerogenes capsulatus, etc.
• The enzyme lecithinase prod by Cl.welchii
  hydrolyses lecithin present in all cells
  including blood cells, resulting in post-mortem
  hemolysis of blood. There is gross breakdown of
  soft tissues and the alteration of their
  proteins, carbohydrates and fats. Org enter
  mainly thru alimentary canal, resp tract, or thru
  an ext skin wound.
• The fall in O2 conc after death favour bact
  growth and spread. In the absence of protective
  agents, bact spread thru blood vessels using
  protein and carbohydrates as culture media.
• Putrefaction usually follows the disappearance of
  RM. During hot season, it may commence before RM
  has completely disappeared from the lower
  extremities.
• The characteristic features of putrefaction are
• changes in the colour of tissues
• the evolution of gases in the tissues, and
• the liquefaction of tissues.
• (1) Colour changes The 1st external sign of
  putrefaction in a body lying in air is usually a
  greenish discol of the skin over the region of
  the caecum, which lies fairly superficially, and
  where the contents of the bowel are more fluid
  and full of bacteria. The colour results from the
  conversion of Hb of blood into sulphmetHb by the
  H2S formed in the large intestines and escaping
  into the surrounding tissues. The colour appears
  in 6 to 12 hrs in summer and in 1 to 2 days in
  winter.

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• The green discol then spreads over the entire
  abdomen, ext genitals and then patches appear
  successively on the chest, neck, face, arms and
  legs. The patches then becomes dark-green and
  later purple and dark-blue.
• The superficial veins esp over the roots of the
  limb, thighs, asides of abdomen, shoulders, chest
  and neck are stained greenish brown or
  purplish-red due to the hemolysis of RBC, which
  stains the wall of the vessel and infiltrates
  into the tissue, giving a Marbled appearance.
  This occurs soon, but is prominent in 36 to 48
  hours.
• The earliest internal change is a reddish-brown
  discoloration of the inner surfaces of vessels,
  esp of aorta. Internally, decomposition proceeds
  more slowly than the surface.
• (2) Development of foul-smelling gases The
  complicated proteins carbohydrates being split
  into simpler compounds of amino acids, ammonia,
  CO2, H2S, methane and mercaptans. The gases are
  non-inflammable in the early stages, but as the
  decomposition progresses, enough of H2S is
  formed, which can be ignited to burn with a blue
  flame. Gases collect in the intestines in 6 to 12
  hrs in summer, and the abdomen becomes tense and
  distended. On opening the abdomen, the gas
  escapes with a loud explosive gas. Due to
  presence of gas in the abdomen, the diaphragm is
  forced upwards compressing the lungs heart, and
  blood-stained froth exudes from the mouth and
  nostrils (post-mortem purge), which can be
  mistaken for the bleeding following ante-mortem
  injury.
• Gas bubbles accumulate in tissues, causing
  crepitant, sponge-like feeling which soon begins
  to distend the body. From 18 to 36 or 48 hrs
  after death, gases collect in the tissues,
  cavities and hollow viscera under considerable
  pressure, and the features becomes bloated and
  distorted.

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