POST MORTEM CHANGES Methods of estimating time 3 following heads Immediate Early Late Immediate Changes Insensibility No response to sensation Touch, pain, temperature TEST: flat EEG

Loss of voluntary power Cessation of respiration Complete stoppage: 3 mins Thorough auscultation for breath sounds Upper part of chest Larynx For a minimum of 5 mins, confirms cessation of breathing. Other test: Feather test no movement of feather in front of nose Mirror test no moisture of breath on the mirror Winslows Test no movement of water surface (in bowl) kept on the chest.

Cessation of circulation Complete absence of heart sounds; > 3-5mins Flat ECG; > 5 mins Other test: Ligature test Distal to ligature, no congestion. Fingernail test No Capillary refilling Diaphanous test Icards Test

Early Changes Primary Flaccidity of the Muscles Muscles lose tonicity. Flaccid, loose and lax. Although physically capable of responding to electrical/ mechanical stimuli.

Postmortem Stiffening (Rigor Mortis) Rigor Mortis ATP is needed to remove head of myosin from actin, and this cause relaxation of the muscle. Depletion of ATP - Prolonged contraction. Onset: 1-2 hr Gradually developed : 6-12 hr Maintained : 12 hr Gradually passed off : 12 hr

Postmortem Hypostasis (Livor Mortis) Livor MortisI Cessation of circulation BP dropping flow slowing and gradually stopped pooling of blood gravitational force pulling down the Red Blood Cells containing haemoglobin (either Carboxyhaem or Oxyhaem). Pooling at the capillary-venous region. Give rise to the reddish purple discoloration. Starts: 1-2 hr after death. Complete: 6-12 hr Differences between Postmortem Hypostasis VS Antemortem BruisesPOSTMORTEM HYPOSTASISBRUISES

Lowest parts of the body (Gravitational dependent parts)Anywhere (near injury marks)

Well-defined marginIll-defined

Blanch with pressure; OR,Whittish at the area pressed with pressureNo blanching with pressure

No swelling at the area or adjacent areaThere is swelling

Due to Gravitational Pooling of Blood at the CapilloVenous DistensionExtravasation of Blood from vessels due to Injury

Postmortem cooling (Algor Mortis) Occurs due to: Cessation of energy production; Inactivity of the heat regulating Centre after somatic death. Loss of heat from body by conduction, convection and radiation. Factors affecting Algor Mortis: Environmental temperature; Air movement; Well ventilated room will cool more rapidly Humidity; damp air fasten heat loss Cadavers body built; Clothing; Age and Sex : Children and elderly loss heat easily Bigger BSA/ Body Volume ratio. Female retain heat longer.

The curve of cooling pattern is sigmoid: Initial phase PLATEU PHASE: Isothermic phase. Residual energy is being used up to maintain normal body temperature. Including still actively operating Thermoragulation centre. Intermediate phase used up residue energy and inactivated Thermoregulation Centre. Terminal phase Slightly above the line; actively bacterial autolysis activities. Site: Most commonly, Rectum (8-10 cm above anus) Subhepatic (Inferior surface of liver; Core Body Temperature) Ext Audi Meastus

Instrument and Methods of Measurement: Chemical thermometer 10-12 inches long, ranging from 0-50oC. Series of recording at certain fixed intervals, say 0.5-1 hr ly. Average body temperature fall in Tropical country ~ 0.8oC/ hr.

TSD (in hrs) = (Normal rectal temp (36.3 37.8oC) Recorded rectal temperature) / Rate of temperature fall per hour, 0.8oC

Eye changes Cornea: Loss of corneal reflex Opacity of the cornea: due to drying, dust or debris deposition. Delayed, if the lids are closed after death. This initial haziness is transient and passes off, with water washing. After about 10-12 hr of death, permanent haziness due to decomposition. Pupils Loss of pupillary reflex (myosis and mydriasis); Pupils are dilated after death. Soon, during rigor mortis, constricted. Pupils are not circular in shape. Even both pupils are not symmetrical by means of diameter or shape.

Flaccidity of the eyeball: intraocular pressure decreases soon after death. Intraocular pressure formed primarily by the orbital arterial pressure. Tache Noire 2 yellow triangles, on the sclera, each one at each side of the iris. Yellow brown black. Changes in retinal vessels: trucking of blood loss of blood pressure vessels become segmented Pallor of Optic Disk

Skin Changes Pallor (eg: facial) Ashy-white Loses Elasticity Asphyxia congested face, bluish black for sometime Jaundice Yellow discoloration CO poisoning Reddish-pink HCN Reddish-pink

Late Changes The death is the end of dying. It is a spectrum of process not an event. Therefore, while some cells of some tissues are still alive, the other cells may be dying or dead. Putrefaction or Decomposition Final stage of; Dissolution of body tissues. Two process contribute to this decomposition: Autolysis It is brought about by the digestive action of enzymes released by dying cells. Can be prevented by freezing the tissues.

Bacterial action It is more dominant process (compared to the Autolysis) Putrefaction Action of microorganism, Aerobic or anaerobic bacteria. Bowel Clostridium welchii Lecithinase Greenish discoloration of skin of anterior abdominal wall, especially at the region of right iliac fossa; First ever viable sign of putrefaction (bacterial action lysis) Due to caecum as reservoir that rich in bacteria and fluid content; Greenish conversion of haemoglobin -> Sulphmet-hemoglobin Usually appears 12-18 hr (in summer), 1-2 days (in winter)

Gradually, spreading of the greenish discoloration over the entire abdominal wall May be observed by about 24 hr in summer. Greenish Purple Dark-blue

Bacteria largely originate from intestines get infested in the venous system; The blood is haemolysed Give stained to the vessels and adjacent tissue. marbled appearance Becomes prominent at about 36-48 hr is summer. Adipocere Mummification Skeletonisation