General Veterinary Pathology

POST - MORTEM CHANGES

Somatic death

• Somatic death is the death of the body as a whole.
• When respiration and cardiac action have stopped, the animal is said to have undergone somatic death. After death, the cells undergo certain changes (post mortem changes), which a pathologist must have knowledge of to distinguish them from lesions found in disease. By a careful study of a postmortem changes one can determine the probable time of death and this is of great importance in medicolegal cases.
• Factors influencing the rate of postmortem autolysis
• Species of animal: Pig-soft and moist muscle- rapid in onset, Horse-dry and firm muscle-slow in onset
• Organ involved: the degrees of the expression of postmortem changes vary from tissues to tissues. The presence of bacterial flora, enzyme secretions and the availability of moisture and substrates influence the rate of postmortem autolysis. Pancreas-high amount-rapid changes. Fibrous tissue-less amount-slow changes. Retina-most sensitive, separates from choroids. Adrenals, liver, testis-abdominal organs also show autolytic changes.

Putrefaction

Decomposition of tissues brought about by the protein splitting anaerobic saprophytic organisms, results in the formation of gas and variety of foul smelling substances- ammonia, hydrogen sulphide, indol, skatol and putrescent amines-like “putriscience and cadaverine”. The tissue turns black or dark-green as a result of formation of iron sulphide from break down haemoglobin. The common putrefactive organisms are Clostridium spp. normally present in faeces, leads to pronounced postmortem changes in the body like gaseous distension, softening etc. Bacterial flora present in GIT and respiratory tract bring about the post-mortem changes rapidly under favourable conditions.

Sequence of postmortem changes

1. Algor mortis
2. Rigor mortis
3. Livor mortis- hypostatic congestion
4. PM clotting of blood
5. Imbibition of hemoglobin
6. Imbibition of bile
7. PM desquamation
8. PM softening
9. PM discoloration
10. PM distention
11. PM displacement
12. PM rupture of organ and tissue

1. Algor mortis

• Algor mortis is cooling of the body. It commences at or before the stoppage of blood flow. The rate of cooling depends on the following factors:
• External atmospheric temperature
• Air currents
• The thickness of hair coat or wool
• Adiposity of the animal
• Amount of fermentable ingesta in the digestive tract
• Larger animals cool slowly; so also in sheep, with thick wool cooling occurs slowly. Limbs and other extremities cool more rapidly than the trunk. The rate at which post mortem changes takes place depends on the rate of cooling and other factors detailed below:

A. Surrounding atmospheric temperature

• Since the postmortem changes are brought about by enzymatic and bacterial activity, high temperature that accelerates this activity will naturally bring on the post mortem changes soon. So in summer, the carcass putrefies quickly. Cold on the other hand retards the enzymatic and bacterial activity. Freezing and deep freezing may stop the activity completely. Hence, carcasses are in perfect state of preservation under polar ice-caps for considerable length of time.

B. State of the body at the time of death

• Higher the temperature at death, sooner do postmortem changes commence.

C. State of muscular activity of animal prior to death

• In animals, that have been very active prior to death post mortem changes commence quicker. This is found in animals that die in chase. Similarly, animals that are killed or die of strychnine poisoning and in animals that die of tetanus, postmortem changes appear early.

The reasons are

• higher body temperature
• greater production of lactic acid in muscular contractions and exercise
• Size of animal

Since body cools slower and so heat is retained longer in larger animals, postmortem changes appear quicker in them

E. External coverings

• Since thick hair or wool retard heat, dissipation, postmortem changes are seen sooner in thick haired or coated animals
• Fatness of animals
• Fat is a poor conductor of heat and so heat loss in fat carcasses is slow, with resultant speedier onset of postmortem changes.
• Infection of animals
• Widespread bacterial infection, especially septiceamic in character, at the time of death begins on postmortem changes earlier.

The following are the changes noticed after death:

2. Rigor mortis

Rigor mortis is contraction of muscles after death.

This is a contraction of muscles after death so that the joints become stiff and body is rigid. Rigor mortis develops first in those muscles that are very active. e.g heart, palpebral muscles, muscles of the head and neck. Gradually other muscles of the forelimbs, the trunk and the hind limbs, are affected in that order. It passes of also in this order, starting first in the head. Usually, rigor mortis appears in 1 to 8 hrs after death and may disappear from 20-30 hours. The following factors hasten the onset of rigor mortis.

• High atmospheric temperature
• Active exercise- hunting, fighting, racing or struggling
• Strychnine poisoning
• FTetanus

Causes of rigor mortis

• The exact mechanism is not known. After death, there is a great overturn of high energy phosphate bonds in the muscle. Adenosine triphosphate (ATP) which breaks down is resynthesized by the energy derived from glycosis. So long as ATP is present, rigors do not occur. With the exhaustion of glycogen, all of ATP is degraded and rigor occurs, since in the absence of ATP relaxation of muscles cannot occur. For the relaxation of the muscles to occur, a considerable quantity of ATP must be absorbed to the muscle proteins. Hence onset of rigor is delayed in well fed animals with large quantities of stored muscle glycogen. But in starved animals, rigor naturally commences earlier. Subsequently when there is no longer any energy necessary for keeping up the chemical activity in the muscle fibres, rigor passes off.
• Onset of rigor mortis is slow in cold weather and in emaciated and cachectic animals. In the later, it is due to the complete exhaustion of chemical systems producing energy.

3. Livor mortis: Hypostatic congestion is, due to gravity, accumulation of blood in vessels of organs that are found on the lower side of the recumbent animal.

4. PM clot is the coagulation of blood in the vessels after death. Chicken fat is the white clot while current jelly clot is the red clot seen in the clot. PM clot is formed after death of animal.

PM clot	Cow - Heart - PM clot

5. Imbibition of hemoglobin: PM staining is pinkish discolouration of endothelium of larger vessels due to haemoglobin (liberated from lysed erythrocytes) after death.

6. PM imbibition of bile is the yellow pigmentation of the tissue occurring in the vicinity of gall bladder.

7. PM softening is softening of tissues, after death, by the action of autolytic enzymes of the cells and the proteolytic ferments of the saprophytes and infecting bacteria.

8. PM discoloration: Pseudomelanosis coli is staining (blackish / greenish discolouration) of intestines due to formation of iron sulphide (H₂s + Fe from Hb = Iron sulphide) after death of animals.

9. PM bloat / PM emphysema is accumulation of gas in the rumen and intestines due to fermentation of food after death.

10. PM displacement of organs: This may occur following handling of carcass by rolling etc.

11. PM rupture of organ and tissue: This may be attributed to softening and handling but devoid of any inflammatory reaction.

In equine practice, stud fee is payable only on the birth of a live foal. So, the veterinarian may be required to certify as to whether a foal was born alive or dead. The two criteria to be looked for are:

• Does the lung float in water? If it floats the foal was born alive since presence of air renders the lung buoyant. Air can be present in lung only if the animal had breathed and breathing can occur only if the foal was born alive.
• Did it suckle? Presence of milk or curds in the stomach is valid evident that the foal was alive at birth and had suckled.