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Post-Mortem Change - Pathology (view source)
Revision as of 20:59, 13 August 2009
, 20:59, 13 August 2009New page: {{review}} {{toplink |linkpage =General Pathology |linktext =General Pathology |maplink = General Pathology (Content Map) |pagetype =Pathology }} <br> ==Algor Mortis== * Cooling of body ...
{{review}}
{{toplink
|linkpage =General Pathology
|linktext =General Pathology
|maplink = General Pathology (Content Map)
|pagetype =Pathology
}}
<br>
==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:
*# The acidic condtion causes Ca<sup>++</sup> efflux from the sarcoplasmic reticulum, leading to contraction of muscle fibres.
*# 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 [[Thrombosis - Pathology#Introduction|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 - Anatomy & Physiology|gall bladder]].
** Stain nearby tissue like the [[Liver - Anatomy & Physiology|liver]], gut, [[Forestomach - Anatomy & Physiology|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.
[[Image:autolysis.jpg|right|thumb|200px|'''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 [[Intestines Catarrhal Enteritis - Pathology#"Pulpy kidney" Disease|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:
*# The''' whole tissue''' is affected.
*# There is '''no zone of host reaction''' such as hyperaemia.
*# The surface may exude fluid.
*# The cut surface tends to be greasy.
*# 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 [[Clostridium species|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 - Anatomy & Physiology|large intestine]] but also on the surface of tissues in contact with it, e.g.
** The posterior surface of the [[Liver - Anatomy & Physiology|liver]].
** The pancreas.
** Part of the [[Forestomach - Anatomy & Physiology|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 - Anatomy & Physiology|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 - Anatomy & Physiology|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.
# Whitish fly larvae in the mouth.
#* Look like rice grains.
#* Deposited after death and appear within hours.
# Removal of tissue by rats or crows.
# The tip of a protruding [[Oral Cavity - Tongue - Anatomy & Physiology|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 [[Post-Mortem Change - Pathology#Hypostatic Congestion / Livor Mortis|hypostatic changes]], causing pooling of blood in dependent sites.
** Kidneys, [[Liver - Anatomy & Physiology|liver]] and pancreas may similarly be affected by vascular congestion.
* The [[Spleen - Anatomy & Physiology|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.
{{toplink
|linkpage =General Pathology
|linktext =General Pathology
|maplink = General Pathology (Content Map)
|pagetype =Pathology
}}
<br>
==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:
*# The acidic condtion causes Ca<sup>++</sup> efflux from the sarcoplasmic reticulum, leading to contraction of muscle fibres.
*# 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 [[Thrombosis - Pathology#Introduction|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 - Anatomy & Physiology|gall bladder]].
** Stain nearby tissue like the [[Liver - Anatomy & Physiology|liver]], gut, [[Forestomach - Anatomy & Physiology|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.
[[Image:autolysis.jpg|right|thumb|200px|'''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 [[Intestines Catarrhal Enteritis - Pathology#"Pulpy kidney" Disease|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:
*# The''' whole tissue''' is affected.
*# There is '''no zone of host reaction''' such as hyperaemia.
*# The surface may exude fluid.
*# The cut surface tends to be greasy.
*# 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 [[Clostridium species|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 - Anatomy & Physiology|large intestine]] but also on the surface of tissues in contact with it, e.g.
** The posterior surface of the [[Liver - Anatomy & Physiology|liver]].
** The pancreas.
** Part of the [[Forestomach - Anatomy & Physiology|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 - Anatomy & Physiology|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 - Anatomy & Physiology|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.
# Whitish fly larvae in the mouth.
#* Look like rice grains.
#* Deposited after death and appear within hours.
# Removal of tissue by rats or crows.
# The tip of a protruding [[Oral Cavity - Tongue - Anatomy & Physiology|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 [[Post-Mortem Change - Pathology#Hypostatic Congestion / Livor Mortis|hypostatic changes]], causing pooling of blood in dependent sites.
** Kidneys, [[Liver - Anatomy & Physiology|liver]] and pancreas may similarly be affected by vascular congestion.
* The [[Spleen - Anatomy & Physiology|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.