12.4 POSTMORTEM AUTOLYTIC AND
DECOMPOSITION CHANGES
Postmortem autolysis and decomposition is accelerated
under the following conditions:
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Elevated environmental and body temperatures.
Increasing time interval from death to necropsy.
Where bacterial pathogens were the cause of death,
they may also hasten the rate of autolysis after death
i.e. clostridia, anthrax.
Body condition - fat animals and those with a dense
hair coat will autolyse more rapidly.
Tissues with greater cellular concentrations of
proteolytic enzymes (gut, gall bladder and pancreas)
and those with naturally high levels of bacteria (gut)
will undergo decomposition more rapidly than other
tissues in the body.
Abomasal rupture - Postmortem digestion by stomach
acids may cause breakdown of the abomasal wall and
release of contents into the abdomen. Antemortem
rupture of an abomasal ulcer would be accompanied by
signs of acute peritonitis - fibrin, pus, fluid and septic smell
would be present.
Absence of rigor mortis - sometimes absence
of rigor mortis is taken as a sign of severe septicaemia
such as in anthrax. However, rigor mortis can be quite
variable in onset, duration and severity and may be easily
missed. Apparent absence of rigor mortis may not have
any significance at all.
Bile imbibitions (bile leakage) - bile is very caustic and
after death it may leak into the duodenum (via the bile
duct) causing the duodenum and sometimes proximal
jejunum to dilate, become thin-walled and develop a
distinct dark green colour. Bile may also stain the surfaces
of organs in contact with the gall bladder.
Bloat - well conditioned animals can bloat quickly after
death and develop signs resembling true bloat, such as
congestion of the head and neck and an oesophageal
bloat line if post mortem bloating occurs before blood
coagulates.
Blood filled visceral organs - muscle contraction
associated with rigor mortis, may force blood from the
limbs centrally into the viscera, especially into the lungs
and liver, causing them to look engorged with blood.
Bloody discharge from the nose - this may be due to
nasal congestion at death and rupture of vessels, which
occurs normally as autolysis proceeds. Nasal and
pulmonary lesions may also cause this and should be
investigated.
Corneal opacity - this is from drying of the exterior
surface and absorption of aqueous humor by the
interior surface, and commences after 12 to 24 hours post
mortem.
Elevated core body temperature - this is not necessarily
an indication of hyperthermia - core body temperature
normally elevates considerably after death in large, fat,
hairy or otherwise well insulatedcattle. However, it usually
takes a few hours before the distinctly high core
temperatures (=43.0oC) and the pink flesh of heatstroke
occur.
Haemoglobin imbibition - lysis of red cells and release of
haemoglobin results in diffusion to surrounding tissues.
This results in pinkish to reddish colouration of tissues. It
begins in or near blood vessels - the pigment leaching out
into surrounding tissue giving a feathered appearance. It
occurs earliest in the large arteries and outer surfaces of
visceral organs adjacent to blood vessels, but later all
tissues become affected.
Intussusception of small intestine - after death, ongoing
peristalsis may cause the intestine to telescope on itself.
Congestion may be present but there is no oedema,
haemorrhage or fibrin (which would be present along with
other signs of obstruction if the intussusception occurred
while the animal was alive).
Livor mortis- after death gravity pulls blood into the
lower parts of the carcass. This can cause distinct surface
patterns on organs. The condition is known as livor mortis
or hypostasis. The skin on the ventral part of the carcass
becomes coloured red to purple. The lower lung and
kidney are darker, wetter and heavier than an upper lung
and kidney. The lower portions of liver are affected
similarly. There will be paleness where organs have
pressed against each other.
Meningeal congestion - gravity may cause blood to pool
in meningeal vessels especially if the head is positioned
dependently after death. It also occurs with meningitis.
Missing carcass pieces - scavengers of carcasses,
especially rats, foxes and dogs can remove teats, noses
and vulvas in such a way they may look surgically
removed.
Mucosal linear reddening - lines of reddening (tiger
striping) on the bladder, colonic and rectal mucosa is
caused by clotting of trapped blood in the ridges of
mucosal folds in the contracted organ. It is not of
diagnostic significance.
Oesophageal bloat line - this is the line in the
oesophagus formed by anterior congestion and distal
pallor. It is inconsistently found in dead ruminants
developing ruminal tympany and hence is not diagnostic
of antemortem bloat.
Prolapse of the rectum or vagina - this may occur
following normal gas distension of abdominal viscera.
Pseudomelanosis - this is gray to black colouration of the
surface of tissues or organs in contact with the intestines.
The intestine itself and the liver, spleen and kidney in
contact with the intestine are commonly affected. It occurs
when autolysis is advanced and bacterial breakdown of
haemoglobin produces hydrogen sulphide.
Pulmonary congestion - reddening of the lungs from
congestion is a common post mortem change and should
not be mistaken for pneumonia. If the lower lung is
affected, it is from gravitational pooling of blood (livor
mortis); if both lungs are affected it is from the forcing of
blood into the lungs which may be the result
of rigor mortis or bloat forcing blood from other parts of
the carcass into the thorax. Pneumonia should be
diagnosed by feel not by colour. Lungs with pneumonia
feel firm - they are like rubber (some viruses,
mycoplasmas) or like liver (other viruses and bacteria).
Pulpy kidneys - this is autolytic change causing the
cortices of the kidneys to become pale and mushy while
the medulla usually looks normal. This is seen mainly in
sheep, but is a common postmortem change in most
ruminants, especially if they are well fed or environmental
conditions are hot. It is thought to be related to high
glycogen levels in the cortical tubules at time of death. It is
not pathognomonic for enterotoxaemia.
Rumen pH - Rumen contents will continue to ferment and
produce volatile fatty acids post mortem, rumen pH may
not be a reliable indicator of acidosis in animals that have
been dead for several hours.
Ruminal tympany - rapid distension of the rumen is
common after death and is not diagnostic of frothy bloat
unless also full of frothy foam.
Segmental intestinal congestion and diapedesis - large
and small areas of red to blue-black congestion
interspersed among non-congested areas can give a
bizarre segmented appearance to the intestine. It is caused
by the variable settling and clotting of blood in the
intestinal wall as peristalsis variably subsides throughout
the length of the intestine. The congested segments may
fill with bloody fluid, leaked from mucosal vessels as
they breakdown over time (diapedesis). These changes
should not be diagnosed as haemorrhagic enteritis unless
accompanied by necrosis, oedema, ulceration or fibrin at
the sites of discolouration, and swelling and oedema in
draining mesenteric lymph nodes.
Sloughing of the rumen mucosa - this occurs normally
within an hour of death - the exposed submucosa may
look pale if the animal has been bled out or intensely red
if not. It should not be regarded as evidence of rumenitis
associated with ruminal acidosis unless there is oedema,
exudate or haemorrhage present in which case the
mucosa is less likely to slough off.
Swelling of the ventral neck and brisket - oedema and
emphysema around the front of the shoulders, at the
thoracic inlet and along the ventral neck may occur in
rapidly decomposing carcasses. It may smell sickly sweet
like blackleg or malignant oedema but is probably
just post mortem change and should not be misdiagnosed
as a clostridial disease.