Forensic medicine changes after death

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CHANGES AFTER DEATH by ************************************************************ ************ DR. AB. HALIM BIN HJ. MANSAR 1

Transcript of Forensic medicine changes after death

Page 1: Forensic medicine   changes after death

CHANGES AFTER DEATH

by

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DR. AB. HALIM BIN HJ. MANSAR

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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

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Two types of death:

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.

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Death

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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 mydriasis2. 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.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 hours

MINNESOTA CRITERIA OF BRAIN DEATH

1. 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.

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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 heart beat (20).

U.S.A COLLABORATIVE STUDY 1977

Prerequisite:

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.

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PRESIDENTS COMMISSION 1981

In July 1981, the Presidents Commission for the Study of Ethical Problems in Medicine and Biomedical and Behavioural Research proposed a new definition of death. it was called the Uniform Detemination of Death Act and was endorsed by the American Medical Association, American Bar Association, the National Conference of Commissioners on Uniform State Laws, the American Academy of Neurology 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 1985

Prerequisite :Irreparable brain lesion detected by CT scan.

Exclusion :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.

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CONFIRMATORY TESTS : BRAIN DEATH

1. EEG

2. Blood flow study :Conventional angiongram.Isotope.DSADoppler

3. Evoked potential :Brain stemSomatosensory

4. ImagingCT ScanMRI scan

RECOMMENDATIONS:

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.

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.

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CHANGES AFTER DEATH

forensic importance: in relation to the estimation of p.m interval : possible interference with the body : indication as to the COD

1 ) 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 found

variables 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- hypothermia

rate 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

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-The Newton’s Law of Cooling (the rate of cooling is proportional to the difference in T between the body surface + its surrounding) did not apply to the human body-Marshall confirmed the ‘double exponential’ or ‘sigmoid’ shape of the rectal cooling curve-the rate is variable depending on above factors-a chemical thermometer is used to measure rectal T (precaution in possible sexual interference)-The use of Henssge’s nomogram for estimating time since death using a single rectal T-The use of Al Alousi cooling curves for estimation of PMI

2) HYPOSTASIS (Lebam mayat) - AKA p.m lividity, staining, suggilation -when circulation ceases, gravity acts on stagnant blood, pulling to lowest accesible 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 linear marks 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 at death, presence of reduced Hb results in darker tint (eg; congestive, hypoxic deaths)

examples : cherry pink in CO poisoning (OxyHb), drowning (nb; refrigerated bodies) : 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!

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Timing + permanence of hypostasis: 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 when hypostasis is already established

Hypostasis 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 of strangulation

Hypostasis VS Bruising: -regular diffuse engorgement of surface vessels in dependent areas of the body with 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 outside vessels)-problem arise when decomposition sets in

3) 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, converting glycogen to lactate (release E)-RM is initiated when ATP conc. falls to 85% of normal + rigidity of M is at its max. when it declines to 15%-has some use in determing time since death-first apparent in small muscle groups as smaller joints are more easily immobilised-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 fade

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Onset 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 RM

In an average temperate condition, the following may be used as a rough guide:

* 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 hours

Rigor 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 M mass as compared to extensors)-below -5 C stifffening occurs in addition to solidification of subcutaneous fat- true RM may supervene as body is warmed up

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4) POST MORTEM DECOMPOSITION (Perubahan lanjut)

- a mixed process ranging from autolysis of indiv. cells by intern. chemical breakdown to tissue autolysis from liberated enzymes, + from external processes introduced 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 vs temperate regions) : environmental T (moisture) : clothing : COD : immersion : earth burial - estimation of the TOD in a decomposed body is extremely difficult

4a) PUTREFACTION (Pembusukan mayat)

-initially there is discoloration of the abdomen (RIF) where bacteria laden caecum is (36-48 hrs)-marbling (bacterial colonisation of venous system, haemolysis of blood, staining of 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, spleen vs prostate + uterus)- coronaries with atheromatous change may be preserved in decomposed bodies

P.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 where body was found, the weather especially ambient T of the area during which the

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body was discovered, (as maturation of insects are markedly altered by climatic conditions)-the Diptera (including bluebottles, greenbottles + common houseflies) are common 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 on already decomposed flesh, although it is more attracted to garbage + manures than to cadavers

- whole cycle lasts about 14 days (from egg to adults) emphasizing that variations in the ambient T. make considerable differences in the rate of maturation -materials to be collected include maggots, adults, pupae and empty pupae cases (live and fixed)-expert knowledge + strict identification of the species is needed before definite opinions upon min. times since death are offered.

-immersion slows decomposition (lower ambient temp., protected from insect + small animal predators)-decomposition in interred bodies is delayed due to lower T, protection from predators + lacks oxygen.-topography of the burial site vs type of soil-deep burial preserves corpse better than shallow/ clandestine burial as it is colder, excludes air better, + not directly affected by rain-the make of the coffin preserves the body, hence allowing exhumation several years later

4b) 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

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- colours from off-white, to pinkish, grey/ greenish grey dt staining with products of decomposition-smell of earthy, cheesy + ammoniacal -favourable conditions include moisture + warmth-anaerobes such as Cl. perfringens produce lecithinase, facilitates hydrogenisation + hydrolysis

-medicolegal significance; it allows the form of the body, facial features (used in identification), even injuries such as bullet holes to be retained in recognisable forms-adipocere formation is grossly visible as early as 3 weeks with 3 months as the typical period

4c) MUMMIFICATION (Mumifikasi)

- like other modes of decomposition, it can be partial/ generalised + can co-exist with them in different areas of the same body-can only occur in dry environment, usually, but not exclusively also a warm place with moving air current-can occur in freezing conditions, partly due to dryness of the air which inhibits bacterial growth -commonly occur in hot, desert zones-there is desiccation, brittleness of the skin, which is stretched tightly across body prominences such as cheekbones, costal margins + hips-skin is discoloured (brown), becomes leathery with secondary colonisation by molds may add patches of white, green/black (adding to p.m artefact)-skin, underlying tissues + internal organs becomes hardened, body is preservedthus allowing possible identification in concealed homicides, mummified fetuses / newborns + major injuries to be preserved

5. 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 which can completely inhibit digestion, gastric motility + pyloric opening

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The following frustrates the use of gastric emptying as a measure of time since death;

a) digestion may continue some time after deathb) the physical nature of the meal has profound effect on emptying time i.e solid vs liquidc) the nature of the food i.e fatty food + strong alcohol causes delay in gastric emptyingd) systemic shock/stress can slow / stop gastric motility + digestive juice secretion as well as holding the pylorus firmly closed

* what is valid is the nature of the last meal which is useful in establishing the TOD

6. THE USE OF VITREOUS HUMOUR CHEMISTRY IN TIMING DEATH

-most useful chemical estimation performed on vitreous fluid for PMI interval is K-serum K rises rapidly after death, impossible to evaluate the status of premortem 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 the degree 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 the values 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

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