Hypo & Hyper Thermia

Dr. Mohammed Saleh Madadin

Forensic Medicine
College of Medicine – university of
 Thermal Injuries

Exposure Exposu
To cold re to
Heat

General Local
effects effects General Local
effects effects
 Definitions

Thermal Death
Internal Heat
Enviromental Heat
Heat Load ( gain)
Heat Loss
1 C = 33.8 F
 Heat loss and Heat gain

Heat is gained:
by conduction from warm air surrounding the body
by the body’s metabolic activity ( liver & muscles)

Heat is lost:

by conduction and radiation to cold air (or water)

by evaporation of sweat from the body surface
Mechanism Of regulation of
body Temp.
Whenever the heat load exceeds the heat
loss body heat rise and body start loss heat
How body decrease temp:
1-vasodilation of bl.v due to inh. Of
symp.centre in post.hypothalamus
2-sweating
3- decrease heat production ( inhibit
chemical thermogenesis)
How body increase temp .?

1- V.C due to stim. Of post.hypothalamus

2- piloerection due to stim. Of sympathetic sys.
3- increase heat production by promoting shivering

Internal heat maintained despite

enviromental variations by
thermoregulatory mech.
 Core body
temperature
>37°C

Thermoreceptors

Hypothalamus
nerves Muscles of
Sweat skin arteriole
glands walls relax
Muscles increase Skin arteries dilate
reduce secretion More blood to the
activity skin.
More radiation &
conduction of heat

More water covers the

skin.
More evaporation

Less heat generated

 Core body
temperature
<37°C

Thermoreceptors

Hypothalamus nerves
Muscles of
nerves Sweat skin arteriole
glands walls
Muscles decrease constrict Skin arteries
constrict
shivering secretion Less blood to the
skin.
Less radiation &
conduction of heat

Less water covers the

skin.
Less evaporation
More heat
generated
 Hyperthermia

Systemic hyperthermia
Endogenous \ Febrile hyperthermia
Exogenous\ non-febrile hypothermia
Heat Cramps
Heat Exhaustion ( Heat prostration)
Heat Syncope ( Heat collapse)
Malignant hyperthermia
 Heat Stroke

Increase in body temp. above 41C in

presence of environmental heat.

ability to cool the body can no longer

compensate for the heat load
life-threatening condition
hot, dry skin, altered sensorium,
tachycardia, hypotension ,
hyperventilation
Predisposing Factors:
alcoholism, dehydration, obesity,
preexisting disease (cardiac and
neurological), diuretics and major
tranquilizers such as
phenothiazines,tricyclic antidepressants,
and monoamine oxidase inhibitors ,
sympathomimitic e.g cocain and amphet..
Relative humidity , DM
Obese individuals show a greater
susceptibility to heat stroke ….. Why ?
This is due to :
(1) Increased adipose tissue creates
an greater demand on the heart
(2) the fat provides extra insulation
for the body, preventing loss of heat
(3) since metabolic heat is produced
in proportion to the bulk of the tissue
Heat stroke is generally seen in two
settings

1- that involving relatively young

individuals exposed to high
temperatures while undergoing
extreme exertion — military recruits
and football players in training
2- a prolonged heat wave. In this latter
circumstance, affected individuals are
also occur in children left unattended
in automobiles for long periods of time
in the summer

Symptoms of heat stroke may come on

suddenly or be preceded by prodromic
symptoms — nausea, vomiting,
vertigo, muscle cramps, dyspnea, a
feeling of warmth.
increase in heart rate, Paresthesias ,
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Complication:
If lives short time after acute insult :
Pneumonia
Tub. Necrosis of kidney
adrenal Hmg
hepatic necrosis
myocardial fiber necrosis &
subendocardia HMG
If the diagnosis of heat stroke has not
been made prior to death, the
diagnosis is often circumstantial based
on history, exclusion of other causes of
death

If an individual’s time of death is

known and if a rectal temperature
taken shortly thereafter shows
hyperthermia, a diagnosis of heat
stroke can be made
Cause of death in hyperthermia
Cardiac dyasarrythmia and collapse
seizures
Shock

Autopsy finding:
not specific
 Heat acclimatization

tolerance to exercise in heat

Due to Subsequent to repeated bouts
of exercise in a hot environment
The 1ry benefit evident as a reduction
of the incidence or severity of
symptoms of heat illness, and
increased work output concurrent with
reduced cardiovascular, thermal, and
metabolic strain.
in metabolic, biochemical,
 Saunas
Exposure to hot & dry environment
60- 120 C
10 – 30 min.
Core Temp begin to rise 1-3 min. ,
constant increase rate
Once outside temp back to normal (
30 min.)
Sweating the only way to cooling
Pt with severe heart dis. At risk
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 Hypothermia

In the past, injury and death from the

effects of low temperature was
thought to occur almost exclusively
among those subjected to extremes of
climate out of doors.
Now, generally appreciated that
hypothermia was a common and
widespread danger in temperate
climates and indoors.
 Case

In Germany , December 2002 , man

called a police , reporting he found his
disabled GirlFriend lying dead on the
living room Floor.
She lives alone

December
Disabled
Live alone
Either :
1- General
2-Localized

Dry or in water

Considered
Externalhypothermia when temp
parts of body : enviromental
less 35C
Dependent
Internal part : constant temp. ( core
Temp.)
 Case

In December 2002 , man called a

police , reporting he found his disabled
GirlFriend lying dead on the living
room Floor.
She lives alone , last time seen last 2
days
Crime scene Inv.:
The floor was flooded with water
The ambient temp. was 19C
Loss of heat in water faster than in air

The aged and the infants are most

vulnerable

Very high mortality of hypothermia in first

few weeks of life ( relation of surface area
to mass and heat regulation centre
immature)
 Pathophysiology of
hypothermia
Internal temp. regulated by

- Heat production :
metabolism , muscular activity

- Heat loss :
increasing blood flow through skin or
sweating
Brown fat play role in chemical
thermogenesis by increase rate of
metabolism

in children heat production up to 100%

while in adult no brown fat ( 10-15%
heat production)
Circumstances of hypothermia :
- exogenous : environmental (less 10C)
- Endogenous : dis. Of endocrine glands ,
drugs (barb. , diazepam) , mental dis.
- Other :
Age and physique
Social and financial factors
LOW ENVIRONMENTAL
TEMPERATURE:

Critical temp. of air to maintain eqili.

25 C
No specific figure , depend on other
factors
10 C consider to be danger to cause
hypothermia
External winds will worse the effect
HYPOTHYROIDISM
Myxoedema , women , over 70
Drugs
Imipramine , chlorpromazine ,
diazepam , barb.,alcohol
clothing
Women tolerate cold better due to
thick layer of s.c fat
Alcohol tend to aggravate the lowering
of body temp rather than rising ( the
heat generated by alcohol is due
internal combustion which therefore
lowers the temperature of inner core of
the body)

Cutaneous diltation of peripheral

vessels (loss of heat and warm flush
feeling)
Alcohol have a secondary effect
causing incapacity and immobility.
 Mechanism of death

As temp. falls decrease in

dissociation of oxyheamoglobin less
supply of O2 to tissue (most affected
nervous tissue)
utilizing capacity of tissue is reduced
at lower temp., all these depress the
oxidative process in the tissue and
leading to tissue hypoxia
Therefore the immediate cause of
death is circulatory failure
 Clinical Manifestation

36°C -32°C: feeling of being cold,

shivering and constriction of blood
vessels

32°C -24C :dulling of consciousness, a

fall in respiration and heart rate, and a
lowering of blood pressure

Loss of reflexes , cold necrosis ,

Hypothermia can cause
heamoconcentration by:
1- cold diuresis (15C) trigger diuresis
2-leaking of plasma into ECF ( cold
edema)

Hyperglycemia :caused by action of

glucocorticoid , and epinephrine on liver
which resultant depletion of glycogen.
 Case
In December 2002 , man called a police , reporting he found
his disabled GirlFriend lying dead on the living room Floor.
She lives alone , last time seen last 2 days
Crime scene Inv.:
The floor was flooded with water
The ambient temp. was 19C
Women rectal temp. was 16 C

Autopsy :
The tap water temp was 16 C

Rigor fully developed

Hypostasis pink
Frost erythema on her knees
Multiple erosion spots on
gastric mucosa
Autopsy

There may be no signs at autopsy

history may be all-important
If pt admitted to hospital and 'warmed-
up', death may supervene at any time
up to a few days later.
signs of hypothermia: patches of pink
to brownish pink discoloration may be
seen
The color of hypostasis cherry red or
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extremities may be cyanosed or they
may be white
Sometimes the feet are blue to the
ankles, above which is pale.
Oedema may be seen
blistering of the skin
Signs of pre-existing disease
Lesions with hypothermia
ACUTE GASTRIC
EROSIONS(Wischnevsky’s Gastric
lesion):
The stomach mucosa have numerous
shallow ulcers, the floor of each
containing a dark brown plug of altered
blood
the stomach contents sometimes
contain dark acid-affected blood.
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PULMONARY OEDEMA: common but
not specific

PENVASCULAR HAEMORRHAGES:
in the brain, especially in the walls of
the third ventricle, they are not
particularly specific
Microinfarcts are common in many
organs in hypothermia.
 Case
In December 2002 , man called a police , reporting he found his disabled
GirlFriend lying dead on the living room Floor.

She lives alone , last time seen last 2 days

Crime scene Inv.:

The floor was flooded with water

The ambient temp. was 19C

Autopsy :
Women rectal temp. was 16 C
Rigor fully developed
The tap water
Hypostasis temp was 16 C
pink
Frost erythema on her knees
Multiple erosion spots on gastric mucosa

Toxicology And Histology

toxicology : -ve
Histology : Wischnevsky’s spots
Diagnosis Made as Fatal
THE 'HIDE-AND-DIE'
SYNDROME
Also called terminal burrowing
behavior
In some cases of hypothermic death in
that it is associated with the victim
undressing and hiding away from sight
The signs of hypothermia are usually
present
problem then arises as to whether the
victim became hypothermic first,
which led to mental confusion that
 Paradoxical undressing

Perimortem act in wich the victim

removes his clothing
Due to
- Terminal hallucination
- Physiologically when failure of V.C
lead to warm blood flow back to the
skin lead to burning sensation
Biochemical markers of
hypothermia
catecholamines appear in the blood
and then urine in the early stages, but
then decline, as the adrenals become
exhausted.
- There is a variation in the
adrenaline:noradrenaline ratio, all
these changes being manifestations of
stress induced by low temperature
 Hypothermia in Water

70-90 min. to die if immersed in water

4-9C and in 30 min at 0 C

Critical temp. of water to maintain

eqili. 35 C

Thickness of individual S.C fat is most

imp. Factor
Cause of Death
Sudden cooling of the skin const. of
bl.v reflex stim. Of heart incr. bl
pressure and C.O Sudden increase in
work of Lt vent Vent. fibrillation (both
atrial and vent. Ectopic beat common
during 1st few min. of cold imerssion)
reflex disturbance of breathing:
involuntary Controlled breathig lead to
inhl. Of water
 Post immersion Death

Occur following rescue from cold water

Conc. When taken out
Because of continuous drop of temp.
for period of time even if rewarmed
Cause of death : cardiac arrest
LOCAL INJURY DUE TO COLD

There are a number of different clinical

lesions caused by the effect of
prolonged cold on the extremities.

1- 'Immersion foot' and 'trench foot'

refer to damp cold damage lead to
necrosis and gangren
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 Case # 2

In Japan , a morning in January, a

male in his early sixties was found
dead in an outdoor parking area.
The minimum temperature during the
night before he was found dead was
estimated to be 4.0°C.
Autopsy revealed the pinkness of
hypostasis, slight abrasions and
bruises on the face and the
extremities, collapse of the lungs, and
 Expalanation

Hyperacetonemia : occur
in hypothermia

Ubiquitin: one of the