death Flashcards

1
Q

What is death?

A

The irreversible cessation of all integrated functioning of the (human) organism as a whole, mental and/or physical…

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2
Q

Somatic death

A
  • An irreversible loss of a persons sentient personality i.e. cannot respond to sensory stimuli or indicate voluntary movement
  • Reflex nervous activity, spontaneous circulatory and respiratory functions might continue, or be maintained artificially
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3
Q

Cellular death

A
  • Tissues (organs) and cells no longer function or cease metabolic activity i.e. aerobic respiration.
  • Cellular death is not instantaneous, different tissues die at different rates e.g. brain cells die after a few minutes of oxygen deprivation, muscle cells can ‘live’ for many hours, or possibly days after circulation ceases
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4
Q

What happens to the body after death

A
  • Most individuals are cremated or buried
    Burial commonly results in
  • Putrefaction with subsequent skeletalisation
    Burial may also result in
  • Adipocere formation (Corpse Wax)
  • Mummification
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5
Q

Modes of death

A
  • Four principal manners of death:
  • Natural – ~500,000 deaths per year or one person every minute… (UK)
  • Accidental – ~12,000 deaths every year (UK)
  • Suicidal – ~5800 deaths per year in UK
  • Homicidal – ~650 deaths per year in UK
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6
Q

Why do we need to know about the subject

A
  • To aid police investigations into suspicious deaths
  • TOD calculations may allow us to identify potential suspects… Who had the opportunity to commit the crime… if it was a crime…
  • To confirm or refute statements from suspect – Does what our suspects say actually make sense?
  • To aid identification of a deceased individual
  • Especially for skeletal or badly decomposed remains – Why can’t we just use DNA?
  • Link to missing persons reports / last sightings
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7
Q

3 sources of evidence

A

Corporal evidence
- Evidence from the body itself… What does the state of decomposition tell us? He’s all stiff and cold, why is that? What does it tell us?
Environmental & associated evidence
- Evidence from around the body… “The place is full of flies!”
Anamnestic evidence
- Evidence of habits or employment
- “He always puts the bins out on a Monday night, but they weren’t out this morning…”

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8
Q

Methods for estimating TOD

Two principle methods

A
  • Rate methods
  • Plotting changes produced by a process that takes place at a known rate and can be measured or observed with some level of accuracy
  • For example core body temperature determination
  • Concurrence methods
  • Comparison to known events
  • For example known last meal comparison to stomach contents, last sighting, watch stopping, Bins put out and not collected etc…
  • Generally a combination where possible
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9
Q

How does death effect the body?

A

Respiration and circulation cease
- Blood no longer flows and tends therefore to be primarily influenced by the effects of gravity
Capacity for aerobic respiration at a cellular level diminishes as oxygen is used up without replacement
ATP production via all oxygen dependent processes ceases
ATP production continues by anaerobic processes using glycogen stores
- ATP levels fall as glycogen is used up
- Pyruvic and lactic acids produced as by-products
- Cellular pH falls to around pH 6 as a result causing enzymatic changes

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10
Q

At the cellular level

A

Oxidative phosphorylation stops
- Electron transport chain inactivated
- ATP levels drop
Membrane channels not maintained
- Ions (e.g. Na+, Ca2+) and water diffuse in to cells, Potassium diffuses out…
Cells burst
- Lysosomal enzymes released e.g. proteinases, amylase, lipases, nucleases
Enzymes begin to digest cells and cell components
- Organelles, nucleic acids digested
Homeothermic processes cease!

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11
Q

How can we use this

A

Death is a physical process – it follows ‘simple’ physical rules
- The body cools at a defined rate
- Certain chemical changes may occur at a defined rate
There are a number of indicators of time since death
- Body cooling
- Skin colouration
- Livor mortis
- Rigor mortis etc…
But do these have the accuracy we need?
- We need to take many factors into account
- How long has our friend here been buried?

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12
Q

Hypostatis (Livor mortis)

A

• Upon death, circulation stops
• Blood simply stops flowing around the body
• It remains in blood vessels
Blood can still form clots
• Coagulation can occur for up to 60 min post mortem
• After this point, it will generally no longer coagulate and remains liquid
Its probably no surprise that
• As in all things, gravity always wins…
• Blood and other fluids will begin to pool in lowest areas of the body
• Where this is depends upon body positionin
Pattern of pooling depends on the position of the body after death
• Areas of the body pressed against a supporting surface will have compressed vascular channels preventing blood flow
• Lighter coloured areas show where pressure prevented pooling
Where would you expect the blood to settle if a body was:
• On its side?
• Inverted?
• Is our friend here male or female?
The colour of hypostasis
• May give investigators some useful information
• Usually blue-red but can vary greatly even in the same body – Note differences from previous slide
Partly depends on state of blood oxygenation at death
• If hypoxic (low oxygen) appears darker – Reasons?
• If due to CO poisoning appears cherry red…
• Due to high concentration of carboxyhaemoglobin
• Note the clear differences in blood coloration in the blood samples
In Caucasians
• Livor mortis is commonly visible within an hour of death itself
• Some factors may affect its development
In dark skinned individuals (RC3/RC4)
• Livor mortis may not be visible due to a lack of contrast between skin colour and lividity
• Exsanguination and injuries causing significant loss of blood may result in little evidence or livor mortis
• Livor mortis slowly disappears with decomposition

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13
Q

Livor Mortis may begin as little as 15 mins after death
Up until 11 hours PM, it is still possible to alter the patterning of livor mortis, but eventually fat in the body begins to solidify and prevents shifting

A

look at ppt

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14
Q

Rigor mortis

A
  • A result of physio-chemical change in muscle protein
  • Occurs when muscle tissue becomes anoxic leading to cessation of oxygen (ATP) dependent processes
  • Results in extreme stiffness that is capable of supporting the entire body weight in some cases
  • Eventually subsides
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15
Q

Rigor Mortis – Post Mortem changes

A
  • Muscles initially relaxed
  • Primary flaccidity
  • Immediately after death muscles relax
  • Muscles begin to stiffen
  • Muscles may stiffen to such an extent that joints become fixed
  • Efforts to move the joint may result in breakage!
  • Muscles relax
  • Secondary flaccidity
  • Rigor passes off due to decomposition of muscle cell
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16
Q

Muscle

A
  • Two main types:
  • Striated muscle (skeletal muscle – voluntary control)
  • Smooth muscle (intestines, organs etc… ‘Involuntary’ control)
  • Muscles contraction is dependent on ATP
  • Muscle tissue reserves a small amount of ATP but when used, it must be regenerated for continued muscle use
  • Failure to produce ATP means the muscles ‘lock’ into position
17
Q

Muscle movement

A
  • Why is this ATP dependent?
  • Muscle movement achieved by interaction of actin and myosin
  • Almost like a ratchet mechanism
  • Once bound, actin and myosin require energy input to disassociate
  • The myosin head is an ATPase enzyme, which undergoes a conformational change when converting ATP to ADP (by hydrolysis)

look at ppt

18
Q

The sarcomere

A
  • Actin and myosin are arranged in a regimented formation
  • The actin-myosin bridge moves muscle fibres closer together –contracting the muscle
  • The actin-myosin bridge cannot be broken without ATP
  • This is the reason for the development of rigor mortis
19
Q

• Supravitality

A
  • After somatic death, muscle cells do not ‘die’ instantly –they undergo a series of changes:
  • Resuscitation period: The period of time in which recovery of morphological, functional and biochemical parameters is possible (3 –4 min for cardiac tissue, 2–3 hours for skeletal muscle
  • Latency period: Oxygen dependent energy production ceases, anaerobic energy production continues (can be up to 10 hours post-mortem)
  • Survival period: Spontaneous activity of organs & reagibility observed (response to electrical stimulation) approx 13 –15 hours for some skeletal muscle
20
Q

Development of rigor mortis

A
  • All the body’s muscles are affected
  • Typically rigor develops in a sequential order:
  • Smaller muscles (eyelids, lower jaw, neck)
  • Small distal joints (hands and feet)
  • Larger proximal joints (elbows, knees, shoulders & hips)
  • Generally considered to pass in same the order it forms
  • Can be mechanically ‘broken’ by force tearing the muscle
21
Q

Timings of rigor

A
  • Primary flaccidity: 0–7 hours
  • Rigor development: 6 –12 hours
  • These timing are extremely variable and depend upon a number of factors
  • Rigor passes completely after enzymatic action breaks down myosin head structure

look at ppt

22
Q

Factors affecting development

A
  • Temperature:
  • Cold (< 10°C) slows the development of rigor and it may not develop at all
  • Heat speeds the development of rigor, it may be complete and resolved in 24 hours
  • Muscle mass
  • Large musculature slows rigor onset
  • Weak muscles become fixed quicker
  • Rigor may not develop appreciably in small children, the elderly and the emaciated who may lack significant musculature
  • Mode of death may affect development
  • Asphixia and CO poisoning may delay onset of rigor
  • Activity
  • Muscle exertion decreases glycogen and ATP stored in body
  • This may be an important factor when determining TOD in some cases
  • Violent struggle/drowning/convulsions prior to death etc.
  • Electrical Injuries
  • May accelerate development and resolution of rigor
  • Alternating current may cause muscle rapid muscle cycling using up muscle ATP
  • External injuries may help determine if this has occurred
23
Q

Cadaveric spasm

A
  • Instantaneous rigor
  • Uncommon finding
  • Muscles fixed in position at death
  • Most commonly seen in hands
  • Gripping gun during suicide, syringe during overdose or debris during fall
  • Is of interest to the investigator but can be misleading in some cases
  • Associated with
  • Sudden deaths particularly those involving penetrating wounds to the head or cerebral haemorrhage
  • Severe pain, fear, excitement, exhaustion…
24
Q

Decomposition

A

• Different cells ‘die’ at different times
• In fact, decomposition can begin in some tissues,
whilst others are still remain alive
• Mixture of processes:
• Autolysis of individual cells – Liberation of a variety of enzymes as the cell loses structure
• Tissue autolysis by liberated enzymes
• Bacterial and fungal activity (endogenous and exogenous) – Even ‘friendly’ bacteria in your stomach aren’t all that friendly after death!
• Animal activity – Larvae such as maggots and also carnivores and carrion birds

25
Q

Putrefaction

A
  • In this section we will discuss some of the changes that take place during the decomposition of tissue
  • Essentially the process of a complex organism becoming little more than a pile of liquid remains
  • Onset
  • Normally 2-3 days at average UK temperatures
  • Cold inhibits the process and heat accelerates it – As would be expected with any chemical process
  • Will not occur in all environments – Extreme dry, acid etc.
  • Can occur at different rates within the same body
26
Q

Stage 1 decay (Fresh)

A
  • After 2-3 days – Note the discolouration of the lower abdomen
  • Friendly bacteria from intestines begin to break down haemoglobin into the blue/green substance sulphaemoglobin and other pigmented substances
  • Begin to break down the intestine itself
  • Digestive enzymes are able to leach into other parts of the body
  • If in the open flies begin activity
27
Q

Stage 2 decay (Early stage Bloat)

A
  • After 1 weeks or so
  • Generalised spread of bacteria to all moist tissues
  • Causes discolouration that can interfere with hypostasis
  • Spread most efficiently through vasculature, observed as ‘marbling’
  • Some early bloating
  • Blister formation in upper epidermis due to fluid accumulation during decomposition
28
Q

Stage 3 decay

A
  • After 2-3 weeks or so
  • Gaseous by-products of bacterial activity cause swelling
  • Gases force liquids from body
  • Tissues also liquefy and are purged
  • Can be wrongly viewed as ante-mortem injury
29
Q

Final Stages of decay (Active and Advanced)

A
  • Time variable
  • Very dependent on environment and situation
  • Maggot or insect activity can destroy tissues as they secrete a proteolytic enzyme destroying ‘dead’ skin and tissue
  • If intact, skin may turn a reddish–green or even black colour
  • Skin slippage causes shedding of outer layers of fingers & toes
  • Eventually leads to skeletalisation (Dry)
30
Q

Non-standard circumstances

A
  • Adipocere
  • Not very useful forensically
  • Formed in cool, humid, anaerobic environments
  • Body fat can be saponified (turned to soap!) by anaerobic bacteria from around 1 month of death onwards
  • Can last for many years – Older material may be chalky
  • Mummification
  • May be the result of a natural process in which the body is prevented from the standard route of decomposition
  • Extremes of cold, salinity, acidity or extreme dryness may produce this effect
  • Flowing air can also accelerate the drying process
31
Q

Algor mortis

A
  • Considered as the most useful single indicator of TOD during the first 24 hours post mortem
  • Why is this?
  • Only applicable in cool or temperate climates
  • Any thoughts as to why?
  • Methods based on core temperature (intra-abdominal temp) not oral or axillary temp
  • A variety of fun ways for this to be taken…
  • How to take the temperature
  • Requires long 10 –12” thermometer (chemical or digital) with wide range
  • Thermometer inserted 3 –4” and read in situ
  • Rectal temperature taken when appropriate
  • Liver temperature via abdominal stab alternative method
  • Other measurements
  • Ambient temperature including min & max if appropriate
  • Environmental observations e.g. Wet, dry, clothed, naked, in air or water (flowing or still)
  • Other pathological indicators such as blood loss, hypothermia etc.
  • Heat is produced by metabolism and distributed by blood – these both cease at death, but not uniformly!
  • Metabolism continues in organs and muscles
  • Heat is lost through the skin surface by:
  • Radiation: any process in which energy travels through a medium
  • Convection: the movement of molecules/heat within fluids (liquids & gases)
  • Evaporation: is a type of vaporisation of a liquid, that occurs only on the surface of a liquid
  • Heat loss is a physical process so follows physical rules
32
Q

Newtons law of cooling

A
  • The rate of body cooling is proportional to the difference between the temperature of the body surface and its surrounding”
  • However, Newton’s law only really refers to small inorganic (non-living) regularly shaped entities…
  • The human body however is a large, irregularly shaped lump of organic matter
  • Practical observations indicate that a sigmoid curve best describes cooling in real life situations – Why might this be?
33
Q

Factors affecting heat loss

A
  • Be aware… Febrile illness can raise temp by up to 4–5 °C
  • Hypothermia can decrease temp by 10°C in some cases!
  • Initial plateau or lag phase varies in its length (0.5 – 3 h) before linear (Newtonian) cooling occurs
  • Many factors influence heat loss in linear phase
  • Surface area:volume largely dictates cooling
  • Conductive properties of tissues influential
  • Subcutaneous fat proportion
  • Oedema and dehydration effects
    • In general, thin people cool quicker!
  • Heat loss from skin drives cooling
  • Radiation & convection
  • Postures exposing less skin cool slower than those in extended posture
  • Also affected by insulating properties of supporting surface
  • Affected by clothing also
  • Dry clothing reduces heat loss via convection conduction
  • Wet clothing accelerates cooling via evaporation
34
Q

Ambient temperature is clearly a major factor in body cooling

A
  • A body will not cool if ambient temp = 37°C and will rise if >37°C
  • Problematic in tropical regions
  • Problematic in cases where the body is in the vicinity of radiators etc.
  • Very complex in the not unusual case of a person dying in a warm bath
  • The medium
  • If still, warm air may ‘block’ temperature differential for some time
  • Air movement brings fresh, cooler air in to contact with skin, promoting cooling and evaporation… even slight breeze has an effect
  • Bodies in closed, small spaces cool more slowly as transfer of heat is less effective
  • Damp air conducts heat more rapidly so will accelerate cooling
  • The medium in most cases is air, but can also be fluid in some cases
  • Water is a better conductor of heat than air
  • For a given environmental temp bodies cool twice as fast in still water and three times as fast in flowing water
  • Quite complex to account for!
  • So we’ve learned all these facts but how do we use them?
35
Q

Most TOD estimations are based upon…

A
  • Old rules of thumb for body cooling:
  • 37°C –1°C/h + 3 (to allow for plateau)
  • An example
  • Rectal temp = 32, TOD = (37 –32) + 3 = 8 hours ago
  • Any problems with this?
  • A better calculations comes from Henssge…
  • Method of TOD estimation using formula based on actual data, taking into account external factors e.g. Body weight, clothing, air, water
  • Best estimate ±2.8 h, worst ±7 h with 95% confidence
36
Q

Hennssge Nomogram

A
  • Based upon the following:
  • T (rectum) – T (ambient) = 1.25 exp(Bt) – 0.25 exp(5Bt)
  • B = -1.2815 (Body Mass -0.625) + 0.0284
  • t = time
  • A huge nightmare to actually solve
  • To make life easier, we can use a nomogram
  • Basically a very complex graph…
  • Assumes no fever or hyp(o/er)thermia, no external radiation etc.
  • Let’s have a go…
    o At 20:00, a naked body is discovered lying inside a building
     Ambient temp = 12°C
     Rectal temp = 30°C
     Body weight = 80kg
    o What was the time of death?
     According to the nomogram, the rectal temperature suggests death 10hrs ago…
     That puts the TOD at around 10:00
     ±2.8hrs
     Death rounded to be between 07:10 and 12:50
    o The nomogram also allows us to factor in a number of other variables
37
Q

Other changes

A
  • The eye is an interesting organ
  • Unique biochemical structure
  • Isolated from main vasculature (No mixing)
  • Resistant to microbial contamination
  • Decomposes at a slower rate than many other organs
  • Samples can be obtained many hours after death (~120 hours)
    In vivo, ion gradient exist across the eye
  • Selective membrane permeability and active transport maintain difference
  • These cease after death
  • The levels of various ions and bio-molecules revert to unity over time
  • Potassium (K+) is most studied electrolyte for TOD estimation
    Collected with needle and small syringe
  • All vitreous humor collected from both eyes (average result used)
  • A gradient will exist across the vitreous too
  • Other structures must not be disturbed (e.g. retina & iris)
  • If vitreous humor cloudy or brown it cannot be used as it is contaminated by other eye structures or bacteria (respectively)
  • Using simple chemistry the concentration of K+ can be measured – How???
    Data shows linear relationship for rise in vitreous [K+] against PMI, sampled to 120 hours PM
  • Sturners’s regression equation describing this relationship:
  • PMI = 7.14 [K+] -39.1
  • Madea et al (1990)
  • PMI (±20 hours) = 5.26 [K+] – 30.9
  • James et al (1997)
  • PMI = 4.32 [K+] – 18.35
  • All based upon studies of PMI, yet all seem to over-read in real life situations… Just too many variables e.g. [Urea] concentration