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Post-mortem biochemical changes
Israa Kamel Mohamed El Araby
e-mail: israakamel2125@gmail.com

Importance?
PMI
Cause of
death
Survival
period

Bile, bone marrow,
brain, testicle, muscle tissue, liver, synovial and CSF fluids
BLOOD(femoral vein)
Mg, PO4, urea, creat., hypoxanthine, ammonia,…, protines
Vitreous
K, Na, Cl , hypoxanthine
Samples

Vitreous
Energy metabolism continues
for a relatively longer period.
It is a well protected and
isolated fluid.
Stable.
The autolytic process is
slower
well preserved even in cases of
severe head trauma.
Less susceptible to
contamination and putrefactive
changes.
It can be easily obtained.
Blood vitreous barrier:
It consists of three components:
 Tight junctional complexes.
It inhibits passage of high molecular
weight constituents.
 Basal lamina of the vitreo-
retinal junction
It physically blocks the passage of
large molecules.
 Vitreous cortex
the physiochemical characteristics of
the vitreous hyaluronic acid network.

Marked and
progressive rise
More rapidly in
an infant than in
an adult
More in dying
from a chronic
illness than from
an acute illness
Potasium in vitreous

Blood changes
pH
5–5.5
Antemortem
7.35-7.45
Hematocrit
47–78
Antemortem
40–45

Metabolite changes
HypoxanthinePhosphateMagnesium
During tissue hypoxia
including death,
elevated hypoxanthine
concentrations are
found in plasma,
cerebrospinal fluid
and urine.
Hypoxanthine
concentration
increases linearly for
the first 24 hours after
death
Inorganic phosphate
rises within 1hr post
mortem to reach
6.6mmol.L/L by 18 hrs
after death.
(antemortem conc. 0.6–
0.9mmol.L/L
Organic phosphorus
not present
antemortem and
present early
postmortem
Plasma conc. Rise rapidly
after blood
hemolysis.
Its level rises specifically
in salt water drowning
victims and
metamphetamine
poisoning.

EthanolAmmoniaUrea
Creatinine
Uric acid
environmental temp,
septicaemia, and severe
trauma with wound
contamination provide
conditions for
microbial ethanol
synthesis
Urine and vitreous
humour will only
indicate alcohol
ingestion, not
microbial production
of ethanol because
microbes do not
quickly penetrate the
bladder or the eye.
Ante-mortem, ammonia
is rapidly removed
from circulation by the
liver, where it is
converted to urea
The ammonia
produced from amino
acids and tissue
degradation
accumulates over time
as it is not removed by
the liver
The only exception
in a study of post-mortem
blood and pericardial fl,
which found a marked
elevation in conc. in the
blood of delayed
traumatic deaths but not
other deaths
These biomarkers may be
suggestive of prolonged
survival time rather than
PMI
Lactate dehydrogenase(LDH)Aspartate aminotransferase(AST)
Lactatepyruvate (anaerobic
glycolysis)
LDH activity in serum increases
rapidly within a few hours post
mortem followed by a slower
increase for the next two to three
days, reaching its highest
concentration around the fourth
day post mortem.
Red blood cells are the main source
of serum LDH so that its post-
mortem increase must be ascribed
to red blood cell autolysis
Aspartate glutamate
found in the heart and skeletal
muscle, as well as liver, kidney,
erythrocytes, and brain tissue
The amount of AST enz. released
from any tissue depends on the
severity of cellular damage.
Erythrocytes contain high conc. of
AST and haemolysis can elevate
AST conc. in the blood stream.
Linear increase for the first 60
hours post mortem
Protein changes

Methods
Chromatography based methods
2D gel electrophoresis
Mass spectrometry
Death

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Death

  • 1. Post-mortem biochemical changes Israa Kamel Mohamed El Araby e-mail: israakamel2125@gmail.com
  • 3.  Bile, bone marrow, brain, testicle, muscle tissue, liver, synovial and CSF fluids BLOOD(femoral vein) Mg, PO4, urea, creat., hypoxanthine, ammonia,…, protines Vitreous K, Na, Cl , hypoxanthine Samples
  • 4.  Vitreous Energy metabolism continues for a relatively longer period. It is a well protected and isolated fluid. Stable. The autolytic process is slower well preserved even in cases of severe head trauma. Less susceptible to contamination and putrefactive changes. It can be easily obtained. Blood vitreous barrier: It consists of three components:  Tight junctional complexes. It inhibits passage of high molecular weight constituents.  Basal lamina of the vitreo- retinal junction It physically blocks the passage of large molecules.  Vitreous cortex the physiochemical characteristics of the vitreous hyaluronic acid network.
  • 5.  Marked and progressive rise More rapidly in an infant than in an adult More in dying from a chronic illness than from an acute illness Potasium in vitreous
  • 7.  Metabolite changes HypoxanthinePhosphateMagnesium During tissue hypoxia including death, elevated hypoxanthine concentrations are found in plasma, cerebrospinal fluid and urine. Hypoxanthine concentration increases linearly for the first 24 hours after death Inorganic phosphate rises within 1hr post mortem to reach 6.6mmol.L/L by 18 hrs after death. (antemortem conc. 0.6– 0.9mmol.L/L Organic phosphorus not present antemortem and present early postmortem Plasma conc. Rise rapidly after blood hemolysis. Its level rises specifically in salt water drowning victims and metamphetamine poisoning.
  • 8.  EthanolAmmoniaUrea Creatinine Uric acid environmental temp, septicaemia, and severe trauma with wound contamination provide conditions for microbial ethanol synthesis Urine and vitreous humour will only indicate alcohol ingestion, not microbial production of ethanol because microbes do not quickly penetrate the bladder or the eye. Ante-mortem, ammonia is rapidly removed from circulation by the liver, where it is converted to urea The ammonia produced from amino acids and tissue degradation accumulates over time as it is not removed by the liver The only exception in a study of post-mortem blood and pericardial fl, which found a marked elevation in conc. in the blood of delayed traumatic deaths but not other deaths These biomarkers may be suggestive of prolonged survival time rather than PMI
  • 9. Lactate dehydrogenase(LDH)Aspartate aminotransferase(AST) Lactatepyruvate (anaerobic glycolysis) LDH activity in serum increases rapidly within a few hours post mortem followed by a slower increase for the next two to three days, reaching its highest concentration around the fourth day post mortem. Red blood cells are the main source of serum LDH so that its post- mortem increase must be ascribed to red blood cell autolysis Aspartate glutamate found in the heart and skeletal muscle, as well as liver, kidney, erythrocytes, and brain tissue The amount of AST enz. released from any tissue depends on the severity of cellular damage. Erythrocytes contain high conc. of AST and haemolysis can elevate AST conc. in the blood stream. Linear increase for the first 60 hours post mortem Protein changes
  • 10.  Methods Chromatography based methods 2D gel electrophoresis Mass spectrometry