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12.4 Postmortem Autolytic And Decomposition Changes

Post-mortem autolysis and decomposition are accelerated under the following conditions:
  • 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 - Post-mortem digestion by stomach acids may cause breakdown of the abomasal wall and release of contents into the abdomen. Ante-mortem 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 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 insulated cattle. However, it usually takes a few hours before the distinctly high core temperatures (43 ºC) and the pink flesh of heatstroke occur. 

Haemoglobin inbibition - 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 carcase. 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 carcase 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 carcase pieces - scavengers of carcases, 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 ante-mortem bloat. 

Prolapse of the rectum or vagina - this may occur following normal gas distension of abdominal viscera. 

Pseudomelanosis - this is grey 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 carcase 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 post-mortem 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 break down 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 carcases. 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.