Death & Changes after Death, Post-mortem Interval.pptx

Death related changes that we can observe as per forensic medicine

1. Death, Changes after Death & Estimation of PM Interval

2. Death Cessation of life, Ceasing to exist- Black’s Law Dictionary It is Complete and irreversible cessation of life It is complete and permanent cessation of vital functions of life It is complete and permanent cessation of functions of ‘ Tripod of life ’ According to Sec. 46 of IPC death denotes death of a human being unless the contrary appears from the context As per Sec. 2(b) Registration of Births & Death Act 1969 death is permanent disappearance of all evidence of life at any time after live birth has taken place

3. Thanatology ( thanatos -death + logos) Scientific study of death and the practices associated with it. Including the study of needs of the terminally ill and their family It is the branch of science that deals with the study of death It is study of death and dying and the psychological mechanisms of dealing with them

4. Types of death Somatic/ Clinical Death/ Systemic death It is the stage of death where body as a whole has died but individually cells and tissues are still alive It is the state of the body that shows complete and irreversible loss of the functions of the brain, the heart and the lungs that is the “Tripod of life” though individually cells & tissue are still alive.

5. Molecular or cellular death Death of cells and tissues at varying period of time after somatic death which may be as late as 6 to 12 hours but most of tissue are dead within 4 hours and brain death in adult human beings may take place in about 5 minutes after stoppage of circulation (clinical death)

6. Brain Death Brain death is defined as the irreversible loss of function of the brain, including the brainstem. An evaluation for brain death should be considered in patients who have suffered a massive, irreversible brain injury of identifiable cause. The three cardinal findings in brain death are coma or unresponsiveness, absence of brainstem reflexes , and apnea Brain death is a clinical diagnosis. A repeat clinical evaluation 6 hours later is recommended A patient certified as brain dead is legally and clinically dead and his other organs can be donated.

7. Three Cardinal Findings Coma/ Unresponsiveness to Pain in all extremities – Nailbed Pressure/ Supraorbital Loss of Brain Stem Reflexes :- Pupil- No response to bright light, mid position (4mm) to dilated(9mm) Ocular movement: - Oculocephalic reflex - If head is moved suddenly and rapidly eyeballs move along with head in brain dead Oculovestibular reflex :- Syringing with cold and hot water of ears produce eye movement and nystagmus in living

8. Brain death No corneal reflex on touch with swab No response after stimulation of the posterior pharynx with tongue blade No cough response to bronchial suctioning Apnea :- All ventilatory support is temporarily removed and Pco 2  levels are allowed to rise. A “positive”  test  is defined by a total absence of respiratory efforts under these conditions .

9. Brain Death (Cont) Evaluate the irreversibility and potential causes of coma Conduct and document the first clinical assessment of brain stem reflexes; Observe the individual during a defined waiting period for any clinical inconsistencies in the diagnosis of brain death Conduct and document the second clinical assessment of brain stem reflexes Perform and document the apnea test Perform confirmatory testing, if indicated Certify brain death; and withdraw cardio-respiratory support or Continue with cardiorespiratory support and Proceed with organ donation.

10. The determination of brain death requires the identification of the proximate cause and irreversibility of coma. Severe head injury, hypertensive intracerebral hemorrhage, aneurysmal subarachnoid hemorrhage, hypoxic-ischemic brain insults and fulminant hepatic failure are potential causes of irreversible loss of brain function. The physician should assess the extent and potential reversibility of any damage, and also rule out confounding factors such as drug intoxication, neuromuscular blockade, hypothermia, or other metabolic abnormalities that cause coma but are potentially reversible.

11. Gordon’s Classification of Death Anoxic anoxia - Defective oxygenation in lungs Obstruction in the respiratory passage Hanging, drowning, strangulation & suffocation etc Anaemic anoxia Reduced oxygen carrying capacity of blood CO poisoning, Histotoxic anoxia Depression of oxygen utilization in tissue Cyanide poisoning Stagnant anoxia Inefficient circulation of blood through tissue Shock following trauma, heat stroke, acute poisoning

12. Modes of Death Coma In death due to cerebral depressants like barbiturate, and other conditions causing coma and leading to death- tumour, haemorrhages etc. Asphyxia Interference in exchange of gases in alveoli leading to reduction of PO2 and rise in PCO2 Hanging, Strangulation, Drowning, Suffocation etc lead to death due to asphyxia Syncope Where cause of death was in heart like coronary heart diseases, cardiomyopathy etc

13. Suspended Animation The conditions in which vital functions are depressed to the extent that the person appears to be dead but recovery is possible and often takes place. Reported in:- Cholera, typhoid state, sunstroke, concussion, drowning, hanging, electrocution, tetanus, convulsions, poisoning by narcotics, surgical shock &anaesthesia, still born infants, snakebite As well as in Yogic trance, Catalepsy, hysteria, and hypothermia. It is a state where metabolic needs of the body are so low that pulse is not palpable, heart sounds not audible respiratory movements not perceptible and reflexes are absent but the person is not dead It is important to recognise this state to prevent premature certification of death

14. Signs Of Death/ Changes after Death Immediate Stoppage of heart & circulation, Stoppage of breathing & chest movements and Stoppage of functions of brain and insensibility, fixation of eyeball, vacant staring look, Absence of corneal & pupillary reflexes, loss of muscle tone and flaccidity Early Changes in skin, eyes, cooling of body, PM lividity, Changes in muscles Late Putrefaction (decomposition)) and modified decompositions like mummification or adipocere formation

15. Immediate Signs of Death Stoppage of heart & circulation Carotid pulse absent Tests for stoppage of circulation Magnus Test:- Applying of ligature to stop venous drainage without occluding artery will cause congestion and swelling of distal part Diaphanous Test:- When palm is viewed against strong light it appears red & translucent during life but pale & opaque with death Icard’s Test:- Subcutaneous injection of Fluorescin a dye causes discoloration of skin around the site if alive Alternate application of pressure on fingernail does not cause alternately white & pink colouration of nailbed Application of heat on a part does not cause erythema of the part or blister formation on burn or scald

16. Stoppage of Circulation/ Respiration No heart sound in apical region when heard interruptedly for 5 minutes Flat ECG recording for 5 minutes No breath sound is heard on placing stethoscope over trachea in neck Surface of mirror becomes dim & clouded due to moisture if kept in front of nose and mouth of living person. This is seen only during winter in most of Indian regions Cotton fibre or feather kept in front of nose and mouth shows movement due to breath Light reflected on a mirror kept on chest shows movement if respiration continues

17. Functions of the Brain No reaction to painful stimuli Fixed eye balls, Vacant staring look, Corneal and pupillary reflexes absent Abdominal and planter reflexes absent Loss of muscle tone, limbs flaccid Gag or cough Reflex-Absent:- On touching posterior Pharynx and soft palate spasm of glottis & coughing. No electrical activity in brain as determined by EEG Doll’s Eye Movement ( Vestibulo -Ocular Reflex or oculocephalic reflex ) Eye movement Nystagmus on irrigating ear with ice cold / warm water- Absent

18. Early Changes After Death Facial Pallor is seen except in asphyxial death Changes in the Skin Elasticity of skin lost, wrinkle’s do not disappear. Translucent skin soon becomes pale and opaque Primary relaxation of Muscles - Tone is lost Muscles are still alive and respond to electrical S Contact Pallor and Contact Flattening Part of body in contact with ground becomes flattened due to wt of body and pale as bloodless

19. Changes in Eye Intraocular tension falls to zero in about 2 hours and eyeballs appear sunken Retina shows ‘trucking’ -break in to segments blood columns in retinal blood vessels- Reliable sign of death Gradual rise in potassium level in vitreous humour. Taches noires sclerotiques - Triangular area of brownish discolouration on both sides of cornea between two partly opened eyelids

20. Taches noires

21. Cooling of the Body ( Algor mortis ) Normal Body Temperature maintained by heat production / heat loss in a living person at 37.2C. After death body assumes the temperature of the environment as control system is lost During winter months and in cold regions there is a gradual fall in temperature as heat is lost by conduction convection and radiation & evaporation. From this time elapsed since death can be determined By subtracting recorded body temperature from normal body temperature and dividing by rate of cooling time elapsed since death can be calculated

22. Algor mortis For first 2 hours body core temperature does not fall From 3 rd hours after death to 6 hours there is regular fall in body temperature which is about 1.5 C during first 6 hours And 0.9- 1.2 C during next 6 hours. Body reaches the low environmental temperature in about 12 to 18 hours

23. Post Mortem Caloricity Temperature recorded at the time of death instead of falling may continue to rise for several hours in cases of death due to violent muscular exercise or tetanus prior to death, violent asphyxial death , septicaemia , alcohol & strychnine poisoning, pontine/ brainstem haemorrhage , sunstroke , cholera , small pox , yellow fever , rabies , rheumatism , meningitis or injury to brain , liver abscess , peritonitis , nephritis,

24. Factors Modifying the Algor mortis Age Bodies of children and old people cool faster than body of young adults and middle aged persons Condition of the body Well nourished and fatty people cool slowly. Lean built small sized person’s body cools faster Stretched supine bodies cool faster than folded up crouched position bodies Manner of death Body cools faster in death due to chronic wasting diseases Surrounding of body Body kept in small closed room or covered with heavy woollen cloth or quilt cool slowly Body buried cools faster than in air but slower than in water.

25. Post-Mortem Lividity Also called - Cadaveric Lividity , Hypostasis, Suggilation , Post-mortem staining , Livor mortis It is discolouration of skin in the dependent part of body as a result of accumulation of blood in the capillaries and small venules under the influence of gravity. It develops according to the position of the dead body in the most dependent part. In bodies which are suspended it is present in lower part of both lower and upper extremities. In supine bodies it is present on back Distribution of PM Lividity indicates posture of dead body after death Part of body in actual contact which carries the wt remains pale as vessels compressed. Similarly skin compressed by clothing remains pale.

26. Fixation of lividity Lividity is generally noticed as small patches of discolouration about 1 to 2 hours after death in dependent areas. With passage of time these patches coalesce with each other and by six hours the entire dependent area except pressure point is uniformly discoloured If position of body is changed then lividity may disappear up to 3-6 hours appearing in the new dependent part but by 8- 12 hours lividity is fixed due to extravasation of blood pigment and does not disappear though new dependent part may still show areas of lividity Colour of post mortem staining depends on the colour of blood , normally it is coppery red or purple where as it is cherry red in CO poisoning, bright red in cyanide poisoning and death due to cold, and cyanotic in opiate poisoning

27. PM Staining (Cont.) Hypostasis is also present in internal organs and their dependent areas are passively congested Livor mortis like discolouration may appear in the living persons during agonal period if circulation is very sluggish as in cholera, plague, uraemia, morphine poisoning, typhus, and asphyxia. PM Staining may not appear in the body if the body is Continuously changing position like in fast flowing rivers In persons who have bled profusely before death People who are very anaemic

28. Difference Between Lividity & Bruise Lividity in wide area Only on dependent part Uniformly present except pressure points Does not appear elevated on the surface There is no extravasation and cutting of capillaries shows that blood is in side vessels. Entire area is uniformly discoloured . Bruise in localised area Any where Takes the shape of weapon causing Bruises are swelling and are elevated on surface There is extravasation of blood which is dark in colour & clotted and demarcated from the adjacent normal area

29. Rigor Mortis Generalised muscular stiffening which follows primary flaccidity of muscles after death It indicates death of individual muscle cells When rigor is fully developed, the joints of the body become fixed, and the state of flexion or extension of these joints depends largely upon the position of the trunk and limbs at the time of death Rigor involves voluntary and involuntary muscles

30. Cadaveric Rigidity Contraction of the arrectores pilorum muscles during rigor may result in "goose-flesh" or "cutis anserina". The phenomenon is commonly seen in cases of drowning where it is thought to result from an agonal contraction of the muscles. Involvement of the walls of the seminal vesicles by rigor may lead to discharge of seminal fluid at the glans penis . Rigor mortis results from a physio-chemical changes in muscle protein, the precise nature of which is unknown

31. Mechanism of appearance When the muscle tissue becomes anoxic after death and all oxygen dependent processes cease to function, then the level of ATP is maintained by anaerobic glycolysis which results in increasing levels of pyruvic and lactic acids. Eventually, the muscle glycogen is depleted, the cellular pH falls to around 6, and the level of ATP also falls below a critical level at which rigor rapidly develops Muscles maintain the rigor till muscle protein is destroyed by combined effect of autolysis and bacterial action with onset of decomposition. Classically, rigor is said to develop sequentially but this is by no means constant, symmetrical or regular

32. Development of Rigor Ante-mortem exertion usually causes rigor to develop first in those muscles which were used in activity Typically, rigor is first apparent in the small muscles of the eyelids, lower jaw and neck, followed by the limbs, involving first the small distal joints of the hands and feet and then the larger proximal joints of the elbows, knees and the shoulders and hips Although rigor begins to develop simultaneously in all muscles, it completely involves small masses of muscle much more rapidly It is generally accepted that rigor mortis passes off in the same order in which it develops

33. Progression & Disappearance The forcible bending of a joint against the force of rigor results in tearing of the muscles and the rigor is said to have been "broken" . Provided the rigor had been fully established, it will not reappear once broken down by force There is great variation in the rate of onset and the duration of rigor mortis In temperate climates rigor will typically start to disappear at about 36-48 hours after death. However, if the environmental temperature is high then the development of putrefaction may completely displace rigor within 12-18 hours of death. Accelerated putrefaction resulting from ante-mortem septicaemia may also lead to a rapid disappearance of rigor within 9-12 hrs.

34. Factors Affecting Duration When the onset of rigor is rapid, then its duration is relatively short The factors influencing the onset and duration of rigor Environmental temperature- In high temp appears early passes off early Cold temperature appears late and stays longer The degree of muscular activity before death. Exertion before death- onset early disappearance early

35. Duration (Cont.) Built- Thinly built- appears early disappears early. Well built comes late stays longer Age- Does not appear prior to the age of viability . Rigor weak in children, elderly and emaciated Early Onset of Rigor Late onset of Rigor Exhaustive wasting diseases- Cholera, Typhoid, Tuberculosis, Cancer Asphyxial death, CO poisoning Violent death like cut-throat, electrocution, firearm, lightening injuries Haemorrhage Poisoning by strychnine, organophosphate, insulin, KCN Cold, refrigerated cadavers Fatigue, Exhaustion, & Heat Stroke Paralysed muscles, Pneumonia

36. Differences b/w Primary & secondary relaxation of muscles Points Primary relaxation Secondary relaxation Time of occurrence Immediately after death After rigor mortis passes off and decomposition occurs. Death of muscle tissue Has not occurred Molecular death of muscles has occurred. Response to stimuli Responds Does not respond.

37. other external findings Body may still be warm Signs of decomposition are there body temperature closer to normal of 98.4 F Low body temperature

38. ML Aspect of Rigor Mortis It indicates molecular death & ordinarily autopsy performed after appearance of Rigor It indicates time passed since death. It may give an idea if body was moved Conditions simulating Rigor Mortis Cadaveric Spasm or instantaneous rigor Heat Stiffening Cold stiffening Gas stiffening or putrefaction

39. Cadaveric Spasm It is well recognised but a rare phenomenon Some voluntary muscles which were in a state of contraction at the time of death, continue to maintain that state of contraction even after death and do not pass in to the state of Primary relaxation Seen in people subjected to intense emotional and physical excitement at the time of death. The condition may affect a group of muscles of hand or limb or even the whole body The condition merges in to true rigor and ends with secondary flaccidity. Cadaveric spasm can not be faked and tells about cause of death

40. Cadaveric Spasm

41. Diffs b/w Rigor mortis & Cadaveric spasm Points Rigor Mortis Cadeveric Spasm Onset Within 1 or 2 hours after death Instantaneous with death. Muscles involved All muscles of the body are affected gradually Selected voluntary muscles which were in a state of contraction at the time of death. Primary flaccidity Precedes R.M. Does not come in the affected muscles

42. Intensity of rigidity / contraction Comparatively moderate Comparatively very strong Death of muscle Molecular death of muscles occur No molecular death of the muscles Duration of stay About 12-18 hours A few hours , until replaced by rigor mortis. Predisposing factor Nil . It is a normal change after death seen in all cadavers. Excitement , fear, fatigue, exhaustion along with contraction of muscles during death.

43. Body temperature Low Comparatively high Muscle reaction Acidic Alkaline Reaction to stimulus Does not respond Responds Mechanism of formation Break down of ATP below critical level Not known exactly. Medicolegal importance Mostly helps to know the time of death Speaks sometimes about cause of death & sometime about the nature of the death (whether suicidal, homicidal etc.)

44. Heat Stiffening Protein coagulates at 65o C (149oF) and hence human body subjected to heat becomes stiff due to coagulation of muscle protein Stiffness more intense and associated with shortening of fibres resulting in powerful group bending that part or whole body pugilistic attitude

45. Pugilistic Attitude

46. Diff. b/w rigor mortis & heat stiffening Points Rigor Mortis Heat stiffening Degree of stiffness Moderate High Time of formation 1 or 2 to 4 hours after death May be antemortem or postmortem . Formed due to application of heat. Role of heat Atmospheric high temperature enhances the process Occurs at a temperature above 65 degree Celsius

47. Mechanism of formation Due to breakdown of ATP of muscles Due to heat coagulation of muscle protein. External appearance Nothing specific Signs of exposure to heat will be there e.g. burning m blackening, blister formation etc.

48. Cold Stiffening A person dying due to cold or body left in cold or refrigerated (Temperature below 5 oC ) becomes stiff and rigor mortis is suspended till the body again is warmed It is associated with bright coloured patches over body similar to lividity Temperature of the body and the environment is low

49. Gas Stiffening It occurs in bodies undergoing putrefaction due to accumulation of gases in tissue. It also may cause pugilistic attitude as flexors being more powerful group of muscles cause flexion of joints. Signs of decomposition are present along with stiffness. Usually seen during summer months in India

50. Secondary Relaxation of Muscles After about 12-18 hours in summer and 36-48 hours in winter rigor mortis passes off in the same order that it had appeared Muscles again become soft and flaccid. Secondary relaxation may not be detected due to rapid decomposition during summer months but during winter it can be appreciated before the commencement of decomposition. Muscles now do not react to electrical stimulus

51. Decomposition  Disintegration, decay, putrefaction The natural decomposition is a process that recycles nutrients back into the food chain after death and continues till the total destruction of all body part takes place. It is a process of breakdown of complex organic matter of human body in to simpler ones due to combined action of autolytic enzymes and saprophytic micro-organisms Putrefaction follows disappearance of rigor mortis but may commence before rigor mortis has passed off from lower extremities in summer months

52. Stages of Decomposition Five general stages are used to describe the process of decomposition in vertebrate animals: Fresh, Bloat , Active and Advanced Decay , and Dry/Remains The general stages of decomposition are coupled with two stages of chemical decomposition Autolysis and  Putrefaction . These two stages largely contribute to the process of decomposition, and break down the main components of the body

53. Decomposition Decomposition begins at the moment of cellular death, caused by autolysis, the breaking down of tissues by the body's own internal  enzymes , Oxygen present in the body is quickly depleted by the aerobic metabolism and aerobic organisms present. This is followed by anaerobic metabolism and the proliferation of anaerobic organisms, originating in the gastrointestinal tract and respiratory system. They begin to transform carbohydrates, lipids, and proteins, to yield organic acids (propionic acid, lactic acid) and gases (methane, hydrogen sulphide, CO2, CO, phosphorated hydrogen &  ammonia). Also mercaptans The process of microbial proliferation within the body causes greenish discolouration , foul smelling along with bloating of body due to accumulated gas.

54. ORGANISMS CAUSING DECOMPOSITION Most decomposers are   Micro-organisms mainly Clostridium welchii, B.coli, Proteus, Staphylococcus, nonhaemolytic Streptococcus, & Diptheroids Fungi : Penicillium  sp.  Aspergillus terrous , & Eurotium repens   Scavengers Flies- flesh-flies ( Sarcophagidae ) and blow-flies Insects  - Beetles (order Coleoptera ) And other animals as:  Jackals, wolves, foxes, rats,  crows dogs and  vultures. 

55. Fungal colonization of human cadaver

56. Progress of Putrefaction Greenish discolouration in Rt iliac fossa which gradually covers whole trunk and face then limbs Marbling of Skin- veins around shoulder and chest, abdomen and groin become prominent purple-brown network of arborescent markings Gradual bloating of body , face and limbs giving Pugilistic attitude of body due to accumulation of gas in tissue and body cavities also Skin blisters varying in sizes up to 20 cms and loosening of epidermis leaving reddish-green to purple-black appearance of underlying dermis.

57. Internal Decomposition In the beginning autolysis causes partial digestion of pancreas and may cause perforation of stomach or oesophagus. Blood disappears from blood vessels and present in altered putrid state in heart. All internal organs initially look pale oily, soft, and with small patches of trapped gases. Viscera later turns greenish, then brown, dark brown and finally blackish with loss of identity of individual organs which finally liquefy. Lungs putrefy earlier than heart. Prostrate in men and nully parous uterus resists putrefaction

58. Progress of Putrefaction Blood tinged fluid starts flowing from body orifices and also accumulates in body cavities Pressure of gas may push out food matter from mouth or in respiratory passage, faecal matter from anal canal and may cause postmortem delivery or prolapse of uterus Hair & nails may separate on pressure, face is bloated lips swollen eyes may bulge out. Distension is most in loose tissue like scrotum & breast, penis and labias . Distended tongue protrudes from mouth. Maggots are seen crawling from body orifices all over the body and the body becomes soft slippery and blackish. Later the abdomen may burst open and maggots may be seen to have invade all body cavities. Gases escape and decomposing soft tissue collapses

59. Colliquative putrefaction : between 5-10 days Abdomen burst open, protruding stomach and intestine and internal organs are converted into thick, semisolid black mass . The tissues and muscles separated from the bones and fall off. Bones, cartilage and ligaments soften. Skeletonisation is completed by one year in an un-coffined body. Bone decomposition - 3-10 years may be delayed by 25 years. Pungent odours from bones indicates recent bones they are of dark brown colour. Adipocere formation - in 3-6 weeks. Mummification takes 3 months to one year.

60. Internal Factors Affecting Rate Age – Still birth baby slow. Fast after feeding Children fast. Old people slow Sex- Women especially fatty putrefy faster Condition of body - Lean thin, emaciated- Slow Cause of death - Death associated with infection causes faster putrefaction. Death due to wasting diseases, anaemia or poisoning retards putrefaction External injury of the body - either ante or post mortem hastens putrefaction.

61. Adipocere ( Saponification ) A fatty substance of waxy consistency in to which cadaver tissues is sometimes converted It is a modified form of putrefaction in which part of a body or whole is converted Saponification or adipocere formation is a modification of putrefaction characterised by the transformation of fatty tissues into a yellowish-white, greasy, (but friable when dry), wax-like substance, with a sweetish rancid odour . It floats on water, and dissolves in hot alcohol and ether. When heated it melts and then burns with a yellow flame. Ordinarily it will remain unchanged for years

62. Adipocere ( Saponification ) Cont. Adipocere develops as the result of hydrolysis of fat with the release of fatty acids (mostly palmitic acid) which, being acidic, then inhibit putrefactive bacteria. Conversion of unsaturated (Oleic acid) liquid fat in to saturated solid higher fatty acids- palmitic , stearic & hydro stearic acid The low (0.5%) level of free fatty acids in fat at the time of death may rise to 70% or more by the time adipocere is obvious to the naked eye Fat, water and moist hot environment are needed for adipocere formation by putrefactive organisms , of which Clostridium welchii is most active. Adipocere develops first in the subcutaneous tissues, most commonly involving the cheeks, breasts and buttocks . Under ideal warm, damp conditions, adipocere may be apparent to the naked eye after 3- 4 weeks

63. The medico-legal importance of adipocere lies in its ability to preserve the body to an extent which can aid in personal identification and the recognition of injuries . The presence of adipocere indicates that the post mortem interval is at least weeks and probably several months.

64. Mummification Mummification is a modification of putrefaction characterised by the dehydration or dessication of the tissues. The body shrivels and is converted into a leathery or parchment-like mass of skin and tendons surrounding the bone. The internal organs are often decomposed but may be preserved. Skin shrinkage may produce large artefactual splits mimicking injuries seen particularly in the groins, around the neck, and the armpits

65. Mummification Mummification develops in conditions of dry heat, especially when there are hot air currents, e.g. in a desert or inside a chimney . New-born infants, being small and sterile, commonly mummify. The forensic importance of mummification lies primarily in the preservation of tissues which aids in personal identification and the recognition of injuries . The time required for complete mummification of a body cannot be precisely stated, but in ideal conditions mummification may be well advanced by the end of a few weeks

66. Maceration The changes of maceration are only seen when a foetus has been dead for several days before delivery . Normally the changes take about one week to develop. Maceration is the aseptic autolysis of a foetus which has died in utero and remained enclosed within the amniotic sac. Bacterial putrefaction plays no role in the process. The body is extremely flaccid with a flattened head There are large moist skin bullae which rupture to disclose a reddish-brown surface denuded of epidermis. The body has a rancid odour but there is no gas formation Soon after delivery bacterial invasion takes place and normal putrefaction occurs Spalding sign present

67. Post-mortem Interval "The time of death is important and has to be estimated in every autopsy along with cause of death but ‘ Time of death’ is extremely difficult to determine, and accuracy is impossible, so a margin should always be given. At autopsy t he survival interval should also be considered by evaluating the types, severity and number of injuries present and the progress of the inflammatory response and repair taking into account pre-existing natural diseases. Estimation of time since death is done by evaluating ‘Corporal evidence’, i.e. Evidence present in the body. ‘Environmental and associated evidence’, i.e. that present in the vicinity of the body, ‘Anamnestic evidence’, i.e. that based on the deceased's ordinary habits, movements, and day to day activities. All three sources of evidence should be explored and assessed before offering an opinion on when death or a fatal injury occurred.

68. CORPORAL EVIDENCE ENVIRONMENTAL & ASSOCIATED EVIDENCE ANAMNESTIC EVIDENCE Stage ofchanges after death:- cooling, lividity decomposition. Uncollected mail/newspapers Usual activities soot in airway (fire/smoke inhalation) Lights on or off Walking & sleeping patterns Evidence if medical conditions Alarm clock set Eating habits, times, types of food Alcohol/drug levels Food on stove/in refrigerator Appointments Beard/nails/hair Type of clothing day/night Answered/unanswered correspondences

69. Estimation of PM Interval There are two methods for estimating the time of death: The rate method . Measuring the change produced by a process which takes place at a known rate, examples include the initiation and distribution of rigor mortis, the change in body temperature, and the degree of putrefaction of the body. The concurrence method . Comparing the occurrence of events which took place at known times, for example, a wrist watch stopped by a blow during an assault, the extent of digestion of the last known meal, faecal matter in rectum, urine in bladder, clothing, growth of beard, condition in the house like kitchen, TV, Bed. All of these should be taken into consideration and one should not rely on isolated findings Specialized investigation like potassium in vitreous

70. METHOD TYPE INDICATOR Rate Method Rate of drying or discoloration of blood pools Rate Method Rigor Mortis Rate Method PM Lividity Rate Method Cooling of body Rate Method Decomposition Rate Method Flora (plants) around body Rate Method Fauna (insects) around body Concurrence Method Time of last known meal Concurrence Method Stopping of watch (due to trauma/damage) Concurrence Method Making or receiving call on cell, misscall

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