Post-Mortem Change - Pathology

()Map GENERAL PATHOLOGY (Map)

Algor Mortis

• Cooling of body after death.
• Can aid in estimating time of death.

Rigor Mortis

• Rigor mortis is a slow stiffening of the muscles caused by enzymatic activity after death.
• Affect striated muscle.
  • Skeletal muscle.
  • Cardiac muscle.

Process of Rigor Mortis

• There is a burst of metabolic activity as substrates are depleted on the cessation of circulation.
  • Heat is liberated, giving a transient increase in temperature.
  • Glycogen is broken down to lactic acid.
• The lactic acid produced is degradged no further, unlike in the living animal.
  • There is a progressive decrease in muscle pH.
    • Muscle oxygen and ATP is also depleted.
• There are two possible methods by which lowered muscle pH produces contraction:
  1. The acidic condtion causes Ca⁺⁺ efflux from the sarcoplasmic reticulum, leading to contraction of muscle fibres.
  2. The acid coagulates the protein in the muscle cells, producing a kind of muscular contraction.

Onset of Rigor Mortis

Factors

• The time to onset and the degree of rigor mortis expressed by the carcass varies with a number of factors.
  • If the animal has been ill and weak for some time there may be little glycogen stored in the muscles.
    • Since rigor development depends on glycogen, it may a slight, transient phenomenon compared with the normal process.
  • The animal may have been in a state of great muscular activity at the time of death.
    • E.g.
      • Being chased.
      • Suffering muscle spasm, as in tetanus or strychnine poisoning.
    • In this case, ante-mortem spasm may lead straight on to post-mortem rigor.
  • Since it is dependent on enzyme activity, the onset of rigor mortis is influenced by the ambient temperature.

Time Course

• Under normal conditions, rigor develops about 2-8 hours after death, and lasts for a further 36 to 72 hours.
  • The animal dying today would go into full rigor today, and remain in rigor tomorrow.
• Rigor starts to wear off on the third day.
  • Due to further autolysis breaking down the coagulated protein in the muscle fibres.
• If rigor is broken forcibly, e.g. by flexing a limb when it is in rigor, it does not recur.
  • This is because no further coagulation contraction is possible.

Pattern in Body

• Rigor mortis tends to occur first in the muscles that are normally most active.
  • The heart is first to be affected.
    • Causes strong contraction of the left ventricle, which is sufficient to expel the blood it contained.
  • The diaphragm contracts next.
  • The head and neck musculature then follows.
    • The jaw muscles are rich in glycogen, so it may be very difficult to prise open the jaw.
    • Rigor of the muscles of the eye mean the eye is retracted into the socket and appears sunken.
      • It may also appear cloudy since the cornea dries out and appears opaque.
  • The changes then spread to the extremities; first the forelimbs and then the hindlimbs.
    • Affects both the extensor and flexor muscles of the limbs.
      • Due to the relative strengths of these muscles, the net result is towards extension of the stiffening limbs.
        • In an unconfined space, the animal is seen lying on its side with its legs stuck out like posts.
• There appears to be a wave of rigor passing down the body beginning at the jaw and ending with the hindlimbs.
• Rigor tends to wear off in the same way as it begins.
  • Those muscles showing rigor first tending to lose it first.

Interpretation of Rigor Mortis

• If rigor is well developed immediately after death, this may indicate :
  • An increased activity just before death.
  • Some poisoning or disease.
• If rigor comes on imperfectly, this may indicate that the animal was weak or ill before it died.
• Failure of the left ventricle to expel its blood before indicates that the heart did not undergo proper rigor.
  • Seen quite often in toxaemia.

Post-Mortem Clotting of Blood

• Blood coagulates in the vessels - seen in:
  • Large arteries
  • The right ventricle, since it has less contractile power in rigor mortis than the left ventricle.
• Quite distinct in appearance.
  • Red blood cells sediment out and gravitate to the lowest position before clotting takes place.
    • This means that the plasma above the sediment is clear.
  • When the blood clots:
    • The upper portion is quite translucent and resembles chicken fat.
    • The lower portion is intensely red and resembles redcurrant jelly.
• Care must be taken to differentiate between post-mortem clotting of blood and ante-mortem thrombi.
  • In post-mortem clotting, there is no damage to the inner surface of the vessel and the clot can easily be removed.
  • A thrombus is not easily removed from the underlying vascular endothelium.

Hypostatic Congestion / Livor Mortis

• At post-mortem, the lower parts of the body may be reddened compared to the other parts of the body.
• When the circulation stops after death, the blood tends to gravitate in the blood vessels to the lowest point before the blood has clotted.
• May be difficult to appreciate in most species as many have deeply-pigmented skin and are covered in hair or fur.
  • Easily appreciated in the pig.
• Particularly evident the lungs and kidneys once the cadaver has been opened.
  • The more dependent lobe or organ is a much deeper red colour than its counterpart on the opposite side.

Post Mortem Imbibition of Blood

• At post-mortem, the surface of organs throughout the body may be diffusely stained by blood.
• Blood pigment tends to diffuse out of the blood cells after death and through the walls of small vessels.
  • Taken up by nearby tissues - like blotting paper sucking up ink.
• Can be appreciated on the surface of organs where there is leakage of blood pigment from the serosal or capsular vessels into the nearby tissue.
  • Also seen on the surface of other adjacent organs or tissues.
• Post-mortem clots in the large arteries and right ventricle and large arteries undergo autolysis.
  • Stains the walls of the vessels and the tissues in contact with the blood vessels.
• Can be quite extensive.
  • Obscures any ante-mortem colour changes that may have been present.
• Foetuses that have been dead for some time in utero before their expulsion show diffuse discoloration of all tissues due to imbibition of blood.
• Animals dying from a disease that causes intravascular haemolysis, show very early imbibition staining.

Inbibition of Bile Pigment

• One of the earliest local colour changes.
• Bile salts diffuse out of the gall bladder.
  • Stain nearby tissue like the liver, gut, stomach and omentum.
• NOT the same thing as jaundice.
  • Generalised discoloration of tissues due to bile pigments seen in the living animal.

Gaseous Distension of the Alimentary Tract

• The intestines and forestomachs may be grossly distended with gas.
  • May pop out of the initial incision made in the abdominal wall during PME.
• Caused by the continuation of normal bacterial fermentation in the alimentary tract after death.
• Adjacent organs may show surface pallor.
  • Due to the pressure of the distension squeezing blood out of this adjacent tissue.
• If the distension is very great, it may be sufficient to tear the wall of the distended portion, or the diaphragm, allowing herniation of the gut into the thoracic cavity.
  • It is possible to distinguish between a post-mortem tear and an ante-mortem rupture by examining the cut ends of the tear or rupture.
    • Swelling and haemorrhage will be evident in an ante-mortem rupture due to the host reaction to injury of living tissue.
    • Swelling and haemorrhage is absent in a post-mortem tear.
  • It is also possible to distinguish tears and ruptures by where the ingesta has come in contact with the parietal or visceral peritoneal surface.
    • If this occurred ante-mortem, there will be a reaction to its presence.
      • May cling to this surface when attempting to wash it off.
• In intestinal distension, the gas tends to rise to the upper part.
  • When the coils of intestine are straightened out, the
    • Upper portions show distension due to the gas.
    • Lower portions show hypostatic congestion.
  • This patchy congestion of the intestine should not be confused with an inflammatory condition of the gut.

Emphysema

• Invasion by gas producing bacteria.

Autolysis

• Self-digestion of tissue.
• As individual cells die, lysosomal and other enzymes are liberated.
  • Digest the tissue, breaking it down.
• Appears similar to necrosis.
  • Distinguishable on PME as there is no host inflammatory response to autolysis.

Histology/Pig Lung - autolysis(Courtesy of Susan Rhind, University of Edinburgh)

Differences in Tissues

• Particularly marked in the gut and associated glands such as the pancreas.
  • These organs are concerned with digestion in life, and their digestive processes continue unregulated after death.
  • Autolysis proceeds fairly rapidly in these organs.
  • The mucosa of the stomach and intestines may be very soft and come off easily from the submucosa when these organs are opened.
• Other metabolically active tissues also become soft from post-mortem change, e.g. the convoluted tubules of the renal cortex.
  • Particularly prominent in PME of the sheep.
    • Can be difficult to distinguish this appearance from the toxaemic changes seen in pulpy kidney.
  • Also true of other tissues such as the brain and spinal cord.
    • Can become almost fluid in texture.
    • Serious histopathological deterioration.
• Autolysis proceeds at a more leisurely rate in other tissues such as muscle, connective tissue and skin.

Gross appearance

• Fairly similar to degeneration and necrosis.
  • I.e. it is paler than normal.
• Further features include:
  1. The whole tissue is affected.
  2. There is no zone of host reaction such as hyperaemia.
  3. The surface may exude fluid.
  4. The cut surface tends to be greasy.
  5. The internal substance tends to be more fluid.

Histological Appearance

• Can be similar to that of necrosis.

Putrefaction

• May be possible to detect putrefaction from outside the animal from the colour and smell.
• Results from the action of putrefactive organisms.
  • Most of these are anaerobes.
    • Grow best or only in the absence of oxygen.
    • Include the Clostridial group of organisms which are found in the large intestine.

Tissue Degradation

• The body proteins, fats and carbohydrates are attacked by enzymes produced by the putrefactive bacteria.
  • Broken down into simpler substances.
  • End result being destruction of the carcass (or most of it).
• New substances are produced by the action of putrefactive organisms on tissue protein, carbohydrate and fat, including
  • Proteases, polypeptides and amino acids another derived from the protein.
  • Indole, skatole and other phenolic compounds.
    • Some of these have an unpleasant odour.
  • Ammonia is produced from the nitrogen in protein.
    • Turns the autolysing muscle undergoing putrefaction , otherwise acid, towards alkalinity.

The Effects of Hydrogen Sulphide

• Hydrogen sulphide is an important product of putrefaction.
  • Formed from the breakdown of the sulphur-containing proteins.
• This is responsible for two things noticeable about putrefying tissue.
  • Colour
  • Smell

Colour

• Putrefaction produces a greenish or blackish discoloration of tissues.
• Colour is due to the development of blackish particles of ferrous sulphide in the tissues.
  • The sulphide part is due to the development of hydrogen sulphide in the putrefying tissues.
  • The iron part comes from the haemoglobin of the blood.
    • Haemoglobin is acted on in putrefaction by bacteria, which split off the iron at the same time as they produce hydrogen sulphide.
      • Components combine to form ferrous sulphide.
• Discolouration therefore depends on the presence of both blood and bacteria.
  • To reduce the incidence of discoloration, the animal should be bled out as soon as possible after death.
• Discolouration is obscured in most animals by the covering of hair or fur.
  • Except in the pig.
  • May still be easily appreciated by parting the fur and noting the green colour on the skin.
• The greenish colour is most noticeable on the skin nearest to the source of putrefactive organisms.
  • I.e. since organisms are found in the gut, the abdominal wall is greenest.
• Discolouration resembles in some respects the colour due to melanin (the ordinary pigment of hair and skin).
  • Is sometimes called pseudomelanosis.
• Pseudomelanosis occurs not only on the skin on and the large intestine but also on the surface of tissues in contact with it, e.g.
  • The posterior surface of the liver.
  • The pancreas.
  • Part of the stomach wall.
  • The ventral surfaces of the kidneys.
  • The putrefactive bacteria grow through the wall of the intestine present and begin attacking the proteins of these organs.

Smell

• Extremely unpleasant
• Smells like rotten eggs.

The Liver

• The liver is very rich in protein and carbohydrates.
• Easily undergoes putrefaction, by:
  • Extension of the bacteria across the gut.
  • Bacteria growing up the portal vein.
• When bacteria grow up the portal vein, the whole organ is affected rather than just the surface.
  • The bacteria produce gas bubbles.
    • The whole liver becomes soft, greenish-blackish and foamy in appearance.
      • Occurs quite commonly in sheep and cattle, but not often seen in small animals.
      • Focal areas of gas formation occur in other tissues undergoing putrefaction.

Other External Features Occuring Post-Mortem

• Occur post-mortem or very shortly before death in very weak animals.

1. Whitish fly larvae in the mouth.
   • Look like rice grains.
   • Deposited after death and appear within hours.
2. Removal of tissue by rats or crows.
3. The tip of a protruding tongue may be bluish in colour and dry from the clenched jaws.

Agonal Changes

• Occur around the time of death/ time of irreversible circulatory failure.
• Often leads to vascular congestion e.g. in the lungs.
  • May be exacerbated by hypostatic changes, causing pooling of blood in dependent sites.
  • Kidneys, liver and pancreas may similarly be affected by vascular congestion.
• The spleen is particularly susceptible to extreme congestion relating to barbiturate euthanasia.
  • Also seen in animals dying under anaesthesia.
  • Crystal deposition on the endocardium is another common barbiturate associated change.
• Agonal regurgitation of GI contents can also occur resulting in food material being present in the airways and possibly alveoli.