Death Flashcards
Somatic (clinical death)
loss of
,circulation
respiration
.
and
CNSMolecular (cellular) death:
The death of individual organs and tissues of the body
Cessation of Circulation :
Loss of pulsations in big arteries
(carotid or femoral pulsations).
No Blood pressure
Loss of heart beat
Flat line on all leads of ECG for 5 minutes
-
Cessation of Respiration
Apnea
Arterial Blood Gas
Severe hypoxia and hypercapnea not consistent with life (>60mmHg)
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Cessation of brain
permanent cessation of cerebral hemispheres and brain stem functions.
The cerebrum has been referred to as the "higher brain" because it has primary control of Awareness and cognition .
The brainstem has been called the “lower brain,” since it controls spontaneous vegetative functions
(swallowing, yawning and sleep-wake cycles).
Exclusions of death
-where the patient may be under the
effects of drugs e.g therapeutic drugs
or overdoses (e.g. sedatives and hypnotics).
-where the core temperature of the body below 35C.
-where the patient is suffering from severe metabolic or endocrine
disturbances which may lead to severe but reversible coma e.g. diabetes.
Preconditions of diagnosis
The patient must be deeply comatose.
The patient must be maintained on a ventilator
The cause of the coma must be known
Signs of Brainstem death
Apnea test. Positive
Absence of corneal reflex
Absence of pupillary response of bright light.
Absence of gag reflex, spontaneous swallowing , tongue or facial movements.
No oculo vestibular response
Absence of oculo- cephalic response
Investigations
🔵Isoelectric EEG for 60 minutes
in adult, clinically brain dead who is not
hypothermic or intoxicated by drugs known to suppress the EEG.
🔵Absence of cerebral blood flow (scintigraphy and
Trans cranial Doppler)
🔵 PET
The brain stem death should be confirmed by;
two medical experts, each separately
not including any of the transplant team and perform examination twice
24hours apart.
Difficult diagnosis of death
Soon after death.
Hypothermia.
Depressant drugs.
Apparent death.
Suspended Animation “Apparent Death”
slowing of life processes
Slide 19
Hhh
Persistent vegetative
state
(PVS)
loses the higher cerebral powers of the brain but the
functions of the brainstem remains relatively intact.
This condition occur in
massive cerebral infarcts
hypoxic encephalopathy
head trauma
.
Sudden Death
This is unexpected death of apparently healthy individual, or death within 24 hours of terminal disease
Sudden death may occur as a result of
▶️Trauma head injury, burns, electric shock.
▶️Poisoning insecticide CO narcotics or hypnotics ▶️Disease (Natural death)
: when a rapid termination of life develops in clinically silent patient
The great majority of sudden, unexpected natural deaths seen at a medical examiner’s office are due to________
cardiovascular disease
Less common are due to CNS, pulmonary disease and sepsis
Other causes
Congenital heart disease: A.S.D., and V.S.D.
Cardiac tamponade: ruptured infarction or aortic aneurysm.
Rheumatic heart disease. Internal hemorrhage. Fulminating infections.
✅
CNS
Epilepsy
Nontraumatic subarachnoid hemorrhage
Intracerebral hemorrhage
Fulminating meningitis
and encephalitis
Brain tumors
Respiratory system
Asthma.
Pulmonary embolism.
Laryngeal and pulmonary edema.
Pneumonia and bronchopneumonia
GIT
such cases are uncommon, with
possibly the most common entity a massive hematemesis due to esophageal varices complicating cirrhosis of the liver
peritonitis
from a perforated duodenal ulcer or an acute peritonitis
Aspleen massively enlarged due to
undiagnosed leukemia may rupture, causing exsanguinations.
Post mortem changes
1- P.M Cooling (
Algor Mortis) : Mechanism
Stoppage of heat production due to stoppage of oxidative processes and metabolism
The body losses 1-1.5 c/hour
Factors affecting postmortem cooling
Initial temp.
Posture of the body after death. Sex
Age
Surroundings : weather, water , clothes
PM caloricity
heating
the body temperature rises 2-3c then cools as usual
Pontine hemorrhage, asphyxia, infection
Primary flaccidity (Contact flattening):
At the moment of death
complete muscle
relaxation and loss of reflexes occur.
Face acquires a peaceful look
Jaw drops, pupil dilate
The muscles contract by electric stimuli(being in the molecular life stage.)
Rigor mortis start two hours after death.
Small muscles of the face Neck Trunk Upper extremity Legs Finger and toes
Factors affecting rigor mortis
Temp. Muscle bulk. Activity.
Cadaveric spasm :
It
s a condition of muscle contraction involving a group of voluntary muscles related to individuals who are at high levels of emotional or physical stress immediately before death
Cadaveric spasm Mechanism
neurogenic
Secondary Flaccidity
The muscles became soft and flaccid (after R.M.) once again, but don’t respond to mechanical or electrical stimuli.
This stage is synchronous with
the onset of putrefaction
Changes of the Eyes:
Loss of corneal and light reflexes
.
Segmentation of retinal vessels
and pallor of optic disc (starts 15 minutes after death).
Fall of intraocular pressure
results into sinking
and flaccidity of eyeballs (starts 1/2 an hour after death)
cornea becomes cloudy and opaque after 2hours
Taches noire
brownish discoloration of
the exposed sclera appear within 3 hours due to accumulation of cellular debris and dust.
Changes of the skin:
The skin becomes pale and opaque.
due to absence of circulation
looses its elasticity so wounds do not gap.
P.M. Lividity (Hypostasis
or Livormortis
)
Bluish discoloration and staining of the skin and tissue of the most dependent parts of the body
It starts immediately after death due to cessation of circulation. Within one hour It becomes maximum and fixed in about
8 hours
due to blood clotting .
Putrefaction
P.M. Decomposition
It’s the final decomposition of soft tissues leaving nothing except bones.
Putrefaction Mechanism
⏺Autolysis after death certain enzymes
⏺Bacterial action aerobic and anaerobic bacteria present in human body
Rate of putrefaction
Greenish
staining of lower abdomen-rt iliac fossa(1-2 days)
Whole body greenish black staining 1wk.
Burst abdomen and larvae 2wks
Bones attached by ligaments 6months
Separate bones 12months
Factors affecting putrefaction
Environment:
Temp.
Moisture.
Medium
Individual: Vascularity Age.
More bacteria,
Adippcere
fatty areas of bodies submerged in water or buried in wet ground. It replaces putrefaction
Mechanism
Unsaturated fatty acids change to saturated fatty acid by the action of hydrogen derived from water and become hard
It starts three weeks after
submersion and completed after
6 months
Mummification
occurs in death in the desert. It replaces putrefaction. The body becomes dry with brown wrinkled skin. It begins after death and completed after. 3-12 months
MLI of adippocere and mummifaction
Preservation of features.
Time of death.
Denotes long submersion in
adepoccere
Or
death in desert.The anesthesia :
overdose -depression of respiratory center or myocardial depression
Light anesthesia- vagal stimulation.
during induction due to tracheal intubations
during recovery due to traction on viscera.
Hypoxia
Obstruction of air passages
Fire and explosion
Malignant hyperthermia
80%
of patients who developed this problem died
an antidote drug was
–
dantrolene sodium
Elevated potassium after succinylcholine
patients suffering from muscle disease Burn Trauma Spinal cord injury
Local anesthetics
injected into vessels in large amounts, the patient may
experience a
seizure
and
cardiac
arrestThe Investigations of a Case of death under anesthesia:
detailed report
Autopsy of the Victim.
Toxicological analysis of samples taken from the body as early Blood collected under oil.
Ø Alveolar air from lung puncture.
Ø The brain and lungs preserved frozen
