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Forensic medicine changes after death


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Forensic medicine changes after death

  1. 1. CHANGES AFTER DEATH by************************************************************************ DR. AB. HALIM BIN HJ. MANSAR 1
  2. 2. Death: - Defined as cessation of life ie total stoppage of blood circulation and a cessation of coordinated (f) of the organism as a whole. - Permanent stoppage of cardio pulmonary (f) s or cerebral death (stedmaus) - A human body with irreversible cessation of total brain (f), according to usual and customary standards of medical practice, shall be considered dead (Am. Bar Association) - Death occurs when the soul leaves the body. Death on neurological grounds - first criteria DeathTwo types of death: 2
  3. 3. a) Somatic death: • The person irreversibly loses it’s sentient personality • Unable to be aware of (or to communicate with) it’s environment • Unable to appreciate any sensory stimuli • Unable to initiate any voluntary movement b) Cellular death: • State in which the tissues and their constituent cells are dead • They no longer (i)/have metabolic activity • It follows ischaemia and anoxia upon cardiorespiratory failure • Is a process, not an event. • Different tissues die at different rates, cerebral cortex muscle connechive tissues.DEATH ON NEUROLOGICAL GROUNDS – FIRST CRITERIA The first criteria was put forward in early 1966 at CIBA symposium in London. These criteria were used to diagnose brain 1. Complete bilateral mydriasis 2. Complete absence of reflexes; natural and to pain 3. Complete absence of spontaneous respiration five minutes after respirator taken off. 4. Falling BP requiring increasing amounts of vasopressor drug. 3
  4. 4. 5. Flat EEG. Based on these criteria the first heart transplant was performed in October 1967.HARVARD CRITERIA OF BRAIN DEATH (1968)1. Unreceptivity and unresponsivity.2. No movements (observe for 1 hour).3. Apnoea (3 minutes off ventilator).4. No reflexes - fixed dilated pupils - No brainstem reflexes - No spinal reflexes5. Flat EEG (of great confirmatory value) at 5 uv/mm6. No change after 24 hoursMINNESOTA CRITERIA OF BRAIN DEATH1. No spontaneous movement.2. Apnoea (4 minutes off ventilator).3. No brainstem reflexes: Dilated fixed pupils, corneal, Ciliospinal, Dolls, eye, gag, caloric, tonic neck reflex.4. Status unchanged after 12 hours.5. Irreparable brain damage.UNITED KINGDOM CRITERIA OF BRAIN DEATH (1976)1. Conditions: Deep coma, drugs metabolic and endocrine causes, hypothermia excluded. Apnoea. Irremediable structural brain damage.2. Testes: Absent brain stem reflexes, fixed pupils, corneal, caloric test, gag, apnoea test.3. Other considerations: Repeat examination depends on injury. EEG not necessary. Spinal reflexes irrelevant. The Faculties produced another memorandum in 1979 stressing the point that identification of brain death meant death irrespective of 4
  5. 5. heart beat (20).U.S.A COLLABORATIVE STUDY 1977Prerequisite: All appropriate diagnostic and therapeutic procedures done. Drugs, hypothermia and remedial lesions excluded.Criteria: (Present for 30 minutes, at least 6 hours after onset of coma and apnoea).Coma with cerebral unresponsivity,Apnoea,Dilated pupils,Absent cephalic reflexes,Electrocerebral silence.Confirmatory TestAbsence of cerebral blood flow.PRESIDENTS COMMISSION 1981In July 1981, the Presidents Commission for the Study of Ethical Problems inMedicine and Biomedical and Behavioural Research proposed a new definition ofdeath. it was called the Uniform Detemination of Death Act and was endorsed bythe American Medical Association, American Bar Association, the NationalConference of Commissioners on Uniform State Laws, the American Academy ofNeurology and the American EEG Society (22).It stated: An individual who has sustained either,1. Irreversible cessation of circulatory and respiratory functions or2. Irreversible cessation of all function of the entire brain including the brain stem is dead.Absent cerebral function;Deep coma unreceptive and unresponsive.Absent brain stem function;Pupils, corneal, oculocephalic, vestibular, oropharyn-geal reflexes and apnoe.Reversible causes excluded.No change with repeat test.JAPANESE CRITERIA OF BRAIN DEATH 1985Prerequisite : Irreparable brain lesion detected by CT scan.Exclusion : 5
  6. 6. Children under 6. Hypothermia. Drug intoxication. Endocrine and metabolic disorders.Criteria : Deep coma (Glasgow scale 3) Apnoea, confirmed by apnoea test. Fixed pupils larger than 4 mm. Absent corneal, ciliospinal, oculocephalic, vestibular, pharyngeal and cough reflexes.Iselectric EEG: Observation : At least 6 hours.CONFIRMATORY TESTS : BRAIN DEATH1. EEG2. Blood flow study : Conventional angiongram. Isotope. DSA Doppler3. Evoked potential : Brain stem Somatosensory4. Imaging CT Scan MRI scanRECOMMENDATIONS:5.1 That the concept and entity of brain death be recognized and accepted; and that brain death means death.5.2 The diagnosis of brain death is a clinical one and no confirmatory test is necessary. The exception to this is only for children because of the greater ability of children’s brain to withstand damage.5.3 2 specialists who are experienced in diagnosing brain death are qualified to certify.5.4 Doctors involved in organ transplantation are not allowed to certify brain death. 6
  7. 7. 5.5 Hospitals where brain death are certified shall have a committee that functions as coordinating body responsible for general policies, to train and accredit staff, counseling and oversee facilities.5.6 To brain death guidelines should be reviewed every 5-10 years to accommodate new knowledge and contemporary practice. CHANGES AFTER DEATHforensic importance: in relation to the estimation of p.m interval : possible interference with the body : indication as to the COD1 ) COOLING OF THE BODY (Penurunan suhu tubuh) reliable up to 24 hrs after death time of death not time of injury rectal temp. to be taken ASAP when body is foundvariables to be considered : - initial body T - ambient T - activity prior to death - death in sleep - infection - asphyxial deaths - pontine haemorrhage - fat + air embolism - aspirin poisoning - hypothermiarate of body cooling affected by:*ventilation (air movement + humidity) *heavy bed clothes + clothings *infants + elderly (S/A): body dimension *body posture *immersion deaths *gen. body built (body fat) *infestation with maggots 7
  8. 8. -The Newton’s Law of Cooling (the rate of cooling is proportional to the differencein T between the body surface + its surrounding) did not apply to the human body-Marshall confirmed the ‘double exponential’ or ‘sigmoid’ shape of the rectalcooling curve-the rate is variable depending on above factors-a chemical thermometer is used to measure rectal T (precaution in possiblesexual interference)-The use of Henssge’s nomogram for estimating time since death using a singlerectal T-The use of Al Alousi cooling curves for estimation of PMI2) HYPOSTASIS (Lebam mayat) - AKA p.m lividity, staining, suggilation -when circulation ceases, gravity acts on stagnant blood, pulling to lowestaccesible areas, rbc initially (gives bluish red colour of hypostasis), then plasma(dependent oedema contributing to blisters)-initially blotchy, then confluent over dependent areas-obvious within 1/2 hrs, marked about 6 hrs, fixed within 4-12 hrs-pattern depends on posture of body after death-most commonly over the back except over P areas (skin remains white as vasc.channels are compressed over these areas)-in hanging, hypostasis most marked distally (eg. below waist + elbows)-local P can exclude hypostasis + produce distinct pattern eg; irregular linearmarks by folds of bed linen, pattern of fabric from coarse cloth, tight belts,brassiere straps, elastic waist bands, socks, skin folds in the neck of the obese-important in determining position of body after death-of limited value in estimating time since death-in gen; it becomes more pronounced as PMI lengthens-elderlies, infants, anaemia + haemorrhage causes slight staining / none at all-colour may signify underlying problems: depends on state of oxygenation atdeath, presence of reduced Hb results in darker tint(eg; congestive, hypoxic deaths)examples : cherry pink in CO poisoning (OxyHb), drowning (nb; refrigeratedbodies) : brownish red in methHbaemia (cyanide poisoning) : pale bronze mottling in septic abortions (Cl.perfringens) : rain drops punctate pigmentation in arsenic poisoning- colour of hypostasis varies even from different areas of the same body!Timing + permanence of hypostasis: 8
  9. 9. If body is moved into a different posture, the primary hypostasis may either:a) remain fixedb) may move completely to the new dependent zones/c) may be partly fixed + partly relocated- controversy about its ability to undergo subsequent gravitational shift whenhypostasis is already establishedHypostasis in other organs:-hypostasis in the intestines may mislead to mesenteric infarction / strangulation- hypostasis at the back of lungs-within posterior wall of LV (early MI)-Prinsloo + Gordon artefact: haem. post. to oesophagus may mislead to dx ofstrangulationHypostasis VS Bruising:-regular diffuse engorgement of surface vessels in dependent areas of the bodywith horizontal margin vs localised/ circumscribed areas in bruising-fresh bruise may be swollen, raised over surface, a/w abrasions-hypostasis in most superficial layer, bruise is deeper + fixed- to incise the suspect area (whether intravascular/ infiltrating tissues outsidevessels)-problem arise when decomposition sets in3) RIGOR MORTIS (Kaku mayat)-dt ATP breakdown + accumulation of lactate + PO4 in Ms resulting in stiffening +M shortening-ATP is converted to ADP, PO4 is used in phosphorylation reaction, convertingglycogen to lactate (release E)-RM is initiated when ATP conc. falls to 85% of normal + rigidity of M is at itsmax. when it declines to 15%-has some use in determing time since death-first apparent in small muscle groups as smaller joints are more easilyimmobilised-in gen. starting with the jaw, facial Ms + neck, then wrists, ankles, knees, elbows+ hips-within 6 hrs: RM developing- from 6-12 hours: RM at its peak + remains constant up to18 hours-18-36 hours: RM begins to fadeOnset of RM may be accelerated / retarded by many factors;a) feverb) physical activity (exercise) shortly before death (as in assault)c) environmental T, (freezing envir. suspends formation of RM)d) electrocution (Krompecher + Bergerioux)-infants, cachexic + elderlies may never develop RMIn an average temperate condition, the following may be used as arough guide : 9
  10. 10. * if the body feels warm + flaccid, its been dead less than 3 hours*if the body feels warm + stiff, its been dead from 3-8 hours*if the body feels cold + stiff, its been dead from 8-36 hours*if the body feels cold + flaccid, its been dead for more than 36 hoursRigor mortis in other organs ;-iris: modifying pupil constriction/ dilatation p.m-ventricles: simulating LVH-dartos muscles: results in extrusion of semen from urethral meatus-in erector pili muscles: beard growing p.m!Heat + cold stiffening:-the ‘pugilistic attitude’ + opistothonus of a burnt body (flexors have greater Mmass as compared to extensors)-below -5 ° C stifffening occurs in addition to solidification of subcutaneous fat- true RM may supervene as body is warmed up4) POST MORTEM DECOMPOSITION (Perubahan lanjut)- a mixed process ranging from autolysis of indiv. cells by intern. chemicalbreakdown to tissue autolysis from liberated enzymes, + from external processesintroduced by bacteria + fungi from intestines + envir.- it varies from body- body, envir. - envir., even one part of the body to another- divided into subclasses: putrefaction, mummification, adipocere formation,maceration-rate of decomposition depending on variables : climate (tropical vstemperate regions) : environmental T (moisture) : clothing : COD : immersion : earth burial 10
  11. 11. - estimation of the TOD in a decomposed body is extremely difficult4a) PUTREFACTION (Pembusukan mayat)-initially there is discoloration of the abdomen (RIF) where bacteria laden caecumis (36-48 hrs)-marbling (bacterial colonisation of venous system, haemolysis of blood, stainingof the vessel walls) on thigh, sides of the abdomen, chest + shoulders- skin slippage + blister formation (clear, pink, red serous fluid) which leaves,slimy pink epidermis when burst, tattooes made more visible-Gen. gas formation in abdomen, genitalia, neck + face (protrusion of eyeballs,tongue etc) making identification difficult/ impossible-purging of bloody fluids from the orifices-may be heavily blood stained-different rates of decomposition of intern. organs (intestines, pancreas, spleenvs prostate + uterus)- coronaries with atheromatous change may be preserved in decomposed bodiesP.m predators and infestation by maggots (entomology studies)-complex life cycles of the insects may be used to determine at least the min.time since death by studying the stage of maturation-this is modified by a no. of factors including climatic + geographic-used since 18th century (Megnin’s Faune des Cadavres)-information to be made to entomologist include the nature of environment wherebody was found, the weather especially ambient T of the area during which thebody was discovered, (as maturation of insects are markedly altered by climaticconditions)-the Diptera (including bluebottles, greenbottles + common houseflies) arecommon insects found on relatively fresh bodies-the bluebottle (Calliphora viccinia) is the most frequent invader of dead flesh +lay eggs only in daylight, they also lay eggs on the living, esp. in debilitated/wounded victims-the complete cycle lasts about 18-24 days from egg to adults-conversely the common housefly (Musca domestica) prefers to lay eggs onalready decomposed flesh, although it is more attracted to garbage + manuresthan to cadavers- whole cycle lasts about 14 days (from egg to adults) emphasizing thatvariations in the ambient T. make considerable differences in the rate ofmaturation-materials to be collected include maggots, adults, pupae and empty pupaecases (live and fixed)-expert knowledge + strict identification of the species is needed before definiteopinions upon min. times since death are offered.-immersion slows decomposition (lower ambient temp., protected from insect +small animal predators) 11
  12. 12. -decomposition in interred bodies is delayed due to lower T, protection frompredators + lacks oxygen.-topography of the burial site vs type of soil-deep burial preserves corpse better than shallow/ clandestine burial as it iscolder, excludes air better, + not directly affected by rain-the make of the coffin preserves the body, hence allowing exhumation severalyears later4b) ADIPOCERE FORMATION (Adiposer)- p.m conversion of body fat-partial/ irregular/ may be generalised-esp. over the face (cheeks + orbits), breasts, abdominal walls + buttocks-dt hydrolysis + hydrogenisation of adipose tissue, leading to formation of waxy,greasy substance (when recent) or brittle chalky material (months + years)composed of palmitic, oleic, stearic acids together with glycerol- colours from off-white, to pinkish, grey/ greenish grey dt staining with productsof decomposition-smell of earthy, cheesy + ammoniacal-favourable conditions include moisture + warmth-anaerobes such as Cl. perfringens produce lecithinase, facilitateshydrogenisation + hydrolysis-medicolegal significance ; it allows the form of the body, facial features(used in identification), even injuries such as bullet holes to be retained inrecognisable forms-adipocere formation is grossly visible as early as 3 weeks with 3 months as thetypical period4c) MUMMIFICATION (Mumifikasi)- like other modes of decomposition, it can be partial/ generalised + can co-existwith them in different areas of the same body-can only occur in dry environment, usually, but not exclusively also a warmplace with moving air current-can occur in freezing conditions, partly due to dryness of the air which inhibitsbacterial growth-commonly occur in hot, desert zones-there is desiccation, brittleness of the skin, which is stretched tightly across bodyprominences such as cheekbones, costal margins + hips-skin is discoloured (brown), becomes leathery with secondary colonisation bymolds may add patches of white, green/black (adding to p.m artefact)-skin, underlying tissues + internal organs becomes hardened, body is preserved 12
  13. 13. thus allowing possible identification in concealed homicides, mummified fetuses /newborns + major injuries to be preserved5. STOMACH EMPTYING AS A MEASURE OF TIME SINCE DEATH(Kandungan gaster)-this method is too uncertain to have much validity-the effect of a physical/mental shock/stress during the digestion process whichcan completely inhibit digestion, gastric motility + pyloric openingThe following frustrates the use of gastric emptying as a measure oftime since death;a) digestion may continue some time after deathb) the physical nature of the meal has profound effect on emptying time i.e solidvs liquidc) the nature of the food i.e fatty food + strong alcohol causes delay in gastricemptyingd) systemic shock/stress can slow / stop gastric motility + digestive juicesecretion as well as holding the pylorus firmly closed* what is valid is the nature of the last meal which is useful in establishing theTOD6. THE USE OF VITREOUS HUMOUR CHEMISTRY IN TIMINGDEATH-most useful chemical estimation performed on vitreous fluid for PMI interval is K-serum K rises rapidly after death, impossible to evaluate the status ofpremortem K level-in contrast to serum + csf, vitreous K levels rise linearly following death-external factors that influence the validity of the test; sampling T analytical instrumentation body T-the ambient T during PMI is probably the predominant factor in determining thedegree of slope at which the vitreous K conc. increases during the p.m interval-The K conc. from either eye differ by a considerable amount-forcible aspiration from too near the retina, cellular fragments will distort thevalues because the K reaches the vitreous by leaching out from the retina-K higher in persons dying of chronic illness with nitrogen retention (due to pre-mortal electrolyte disturbances in patients with metabolic disorders-the rise in infants is much fasterSturners equation; PMI= 7.14 x K conc. (mmol/l)- 39.1 13