Download GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD):

HYPOTHERMIA:
PART I
Jassin M. Jouria, MD
Dr. Jassin M. Jouria is a medical doctor,
professor of academic medicine, and
medical author. He graduated from Ross
University School of Medicine and has
completed his clinical clerkship training in
various teaching hospitals throughout New
York, including King’s County Hospital
Center and Brookdale Medical Center,
among others. Dr. Jouria has passed all
USMLE medical board exams, and has
served as a test prep tutor and instructor
for Kaplan. He has developed several
medical courses and curricula for a variety
of educational institutions. Dr. Jouria has
also served on multiple levels in the
academic field including faculty member and Department Chair. Dr. Jouria continues to serves
as a Subject Matter Expert for several continuing education organizations covering multiple
basic medical sciences. He has also developed several continuing medical education courses
covering various topics in clinical medicine. Recently, Dr. Jouria has been contracted by the
University of Miami/Jackson Memorial Hospital’s Department of Surgery to develop an emodule training series for trauma patient management. Dr. Jouria is currently authoring an
academic textbook on Human Anatomy & Physiology.
ABSTRACT
When the human body becomes too cold to spontaneously rewarm itself
through normal metabolic procedures, hypothermia occurs. Hypothermia can
range from mild to severe and its symptoms include mental confusion, slow
heart rate, and even death. Since an extreme low core body temperature can
suppress heart and brain function, hypothermia treatment protocols vary from
the treatment of other heart- and brain-related incidents. This course, Part 1
of a 2-part series, provides a detailed explanation of hypothermia and field
treatment protocol.
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Continuing Nursing Education Course Planners
William A. Cook, PhD, Director, Douglas Lawrence, MA, Webmaster,
Susan DePasquale, MSN, FPMHNP-BC, Lead Nurse Planner
Policy Statement
This activity has been planned and implemented in accordance with the
policies of NurseCe4Less.com and the continuing nursing education
requirements of the American Nurses Credentialing Center's Commission on
Accreditation for registered nurses. It is the policy of NurseCe4Less.com to
ensure objectivity, transparency, and best practice in clinical education for all
continuing nursing education (CNE) activities.
Continuing Education Credit Designation
This educational activity is credited for 4 hours. Nurses may only claim credit
commensurate with the credit awarded for completion of this course activity.
Statement of Learning Need
Hypothermia is a leading cause of death in several United States regions.
Cases of profound hypothermia and devastating consequences have been well
documented in the pre-hospital setting. New criteria to determine exposure,
prognosis, even death, and critical treatment modalities is important for
nurses to know when dealing with life-threatening situations.
Course Purpose
To provide professional nurses with advanced learning of hypothermia and
critical interventions to support survival.
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Target Audience
Advanced Practice Registered Nurses and Registered Nurses
(Interdisciplinary Health Team Members, including Vocational Nurses and
Medical Assistants may obtain a Certificate of Completion)
Course Author & Planning Team Conflict of Interest Disclosures
Jassin M. Jouria, MD, William S. Cook, PhD, Douglas Lawrence, MA
Susan DePasquale, MSN, FPMHNP-BC – all have no disclosures
Acknowledgement of Commercial Support
There is no commercial support for this course.
Activity Review Information
Reviewed by Susan DePasquale, MSN, FPMHNP-BC
Release Date: 7/18/2016
Termination Date: 7/18/2017
Please take time to complete a self-assessment of knowledge, on
page 4, sample questions before reading the article.
Opportunity to complete a self-assessment of knowledge learned will
be provided at the end of the course.
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1. The normal adult temperature ranges from 36-38°C, depending
on many internal factors such as:
a.
b.
c.
d.
Wind movement
Circadian rhythm
Humidity
Nature of surrounding environment
2. Which of the following neuronal effector mechanisms activated
by cold stimuli increase heat production?
a.
b.
c.
d.
Shivering
Cutaneous vasodilation
Piloerection Humidity
Sweating
3. Which clinical findings can be seen in patients with mild
hypothermia?
a.
b.
c.
d.
Diminished shivering
Slow stretch reflexes
Stiff muscles and joints
Cold-induced diuresis
4. Which mechanism of environmental heat loss is exemplified by
the dissipation of up to 50 percent of the body’s heat through an
uncovered head?
a.
b.
c.
d.
Convection
Conduction
Radiation
Evaporation
5. Which mechanism of environmental heat loss is exemplified by
excessive sweating?
a.
b.
c.
d.
Convection
Conduction
Radiation
Evaporation
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Introduction
Hypothermia is defined as a pathologic condition wherein the core body
temperature is less than 35°C. It is the opposite of hyperthermia, wherein the
body experiences elevated core temperature due to failed thermoregulation.
Hypothermia
is
due
to
a
cold
stressor
that
overwhelms
the
body’s
thermoregulatory mechanisms and represents a potential medical emergency.
It may be classified by its degree, mild, moderate or severe; or, by its cause,
accidental or intentional (therapeutic). In this course, accidental hypothermia
is the focus of discussion.
There is always a greater incidence of hypothermia in cooler climates;
however emergency medical service providers and other health professionals
must be able to recognize it even in patients on ambient temperatures. Early
recognition of hypothermia and treatment is very critical. Patients with signs
and symptoms of hypothermia must be brought to the hospital as soon as
possible. Here, the pathophysiology of hypothermia is discussed as well as its
field assessment, pre-hospital management and treatment measures, and
possible complications. It is important for nurses and paramedics to be able to
identify the signs and symptoms of hypothermia and treat it accordingly prior
to the arrival of the patient in the hospital or during the pre-hospital care of
hypothermic patients.
Background
In the United States., hypothermia is often caused by prolonged exposure to
external cold temperatures, especially in the winter. The reported cases of
hypothermia reflect those that have resulted in emergency room visits,
although this is not the true number. Nevertheless, the number of reported
cases for hypothermia is increasing, due to growing interest in winter
activities, as well as personal issues with alcoholism, mental illness, and
homelessness.
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The Centers of Disease Control and Prevention (CDC) published statistics of
reported hypothermia cases in areas that experience severe weather,
although other areas with milder winter climates also experience such cases
regularly.1 This is particularly true in milder areas that are subject to rapid
weather changes on a daily basis. Based on the latest U.S. data, the highest
rates of hypothermia occurred in the Midwest and Northwest regions with
Alaska, Maine and Montana having the highest annual rates of hypothermia
cases requiring hospital treatment.2 In urban areas, hypothermia rates are
highest among those that are overly exposed to external cold due to
alcoholism,
illegal
drug
use,
or
psychiatric
illness,
combined
with
homelessness. On the other hand, hypothermia also occurs a lot among those
who frequently engage in outdoor activities such as climbers, swimmers,
rafters, hunters, and campers.
Although they happen, deaths due to hypothermia are relatively uncommon.
The report of one study found that the total inpatient of hypothermic
individuals occurring in the coldest regions of the U.S. is about 12 percent.2
Deaths tend to result from moderate and severe hypothermia, with significant
mortality
rates
despite
hospital-based
treatments.
Hypothermia-related
deaths for the U.S. in the most recent CDC report indicated annual rates
ranging from 0.3 to 0.5 per 100,000 persons, which represented a significant
increase of reported cases.1 The majority of people can tolerate mild drops in
core body temperature (i.e., less than <95°F or 35°C core body temperature)
relatively well, which do not result in significant morbidity or mortality. On the
other hand, moderate hypothermia has been found to be associated with a
higher patient mortality rate. As mentioned previously, deaths are more likely
to occur with severe hypothermia. This is especially true for patients with
comorbid illness, advanced age or with positive blood alcohol levels. Other risk
factors for deaths due to moderate and severe hypothermia are also due to
homelessness and mental illness and addiction disorders.1,2
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According to latest estimates in the U.S., between 2003–2013, there was a
total of 13,419 hypothermia-related deaths with unadjusted annual rates
ranging from 0.3 to 0.5 per 100,000 persons. During the ten-year period,
male victims accounted for 67%; and both males and females aged ≥65 years
accounted for 1.8 and 1.1 per 100,000 population, respectively. Ten percent
of reported deaths from hypothermia had alcohol or drug poisoning as a
contributing factor.1
Pathophysiology
In order to understand the pathophysiology of hypothermia, one must
understand the thermoregulatory mechanisms of the human body. This
section discusses physiological processes and external factors influencing how
individuals respond to freezing conditions.1-4
Thermoregulation ensures that the body maintains its normal core body
temperature of about 37°C. This temperature is also the set point, which
means that temperatures below or above 37°C can seriously harm the body
by affecting its physiological mechanisms. The normal adult temperature
ranges from 36-38°C, depending on many internal factors, such as:

Circadian rhythm

Monthly menstrual cycle (females)

Exercise

Area of measurement (oral, esophageal, maxilla, rectal)
The core body temperature, such as esophageal and rectal, is normally 0.5°C
greater than the oral temperature. Due to the circadian rhythm, it also
fluctuates more or less 0.6°C between the morning and evening. The core
temperature is highest during the evenings and lowest during the mornings.
Women also experience core body temperature changes during their monthly
menstrual cycle. It increases by 0.5°C during ovulation and falls back to
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normal when menstruation begins. It also increases during exercise, rising to
as high as 40°C and falling back to normal after exercise.
When an individual is exposed to cold air in the external environment, the rate
and degree of decrease in the body temperature depends on the following
external factors:

Wind movement of the air

Humidity

The nature of the surrounding environment
This means that generally speaking, a nude individual exposed to dry air
between 13-54°C can maintain a normal body temperature ranging from 3637.7°C. This is only true for dry air since greater wind movement and
humidity can exacerbate the sensation of coldness in the air. Physiological
functions
including
metabolism
dependent, which means that
and
thermoregulation
are
temperature
they only occur when the core body
temperature is at its set point or normal level. The balance between heat loss
and heat production (thermogenesis) determines the normal level of body
temperature or set point. Two regions of the hypothalamus, the posterior
region and the anterior region, control thermoregulation. These regions play a
unique but mutually coordinated role through a feedback mechanism.
The posterior pituitary region is concerned with heat maintenance. It contains
a large number of cold-sensitive nerve cells. These cells act as cold sensors
and are stimulated by the brain cortex when the body comes into contact with
a cold stimulus. Once the cold sensation is registered, neuronal effector
mechanisms that produce heat and reduce heat loss are activated. One
example is the increase in firing rate of these neurons. Other examples are
outlined in the table below.
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Posterior hypothalamic lesions can severely interfere with thermoregulation.
For example, a patient can become severely poikilothermic (temperature
tends to fluctuate), which is followed by a very low body temperature. On the
other hand, the anterior pituitary region is concerned with heat loss. It
contains a greater number of heat-sensitive neurons which also act as
sensors. An elevated blood temperature above the set point is what stimulates
these cells. Once an abnormally high intravascular heat level is registered,
neuronal effector mechanisms that increase heat loss and decrease heat
production are activated. One example is the two- to ten-fold increase in the
firing rate of these nerve cells. Other examples are outlined in the table
below. Anterior hypothalamic lesions can also severely
interfere with
thermoregulation. For example, a patient can become severely warm, with a
core body temperature reaching up to 43°C.
Activated Mechanisms in Response to Cold Stimuli
↑ Heat production
Shivering
Increased muscular activity
Hunger
Increased TSH release
Increased epinephrine release
Increased norepinephrine release
↓ Heat loss
Cutaneous vasoconstriction
Piloerection
Behavior modification (i.e., building fire)
Thermoreceptors
Aside from the hypothalamus and the sensory neurons in the brain, there are
also other thermoregulatory parts of the body. The most notable of these are
thermoreceptors found in the skin. The skin contains both cold and warmth
receptors. The number of cold receptors is ten times more than the warmth or
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heat receptors. As a result, peripheral recognition of temperature is primarily
focused on detecting cool and cold instead of warm temperatures. When the
cold stimulus is encountered, immediate reflex effects are stimulated and
initiate the increase in body temperature through:

Provision of a strong stimulus to cause shivering to increase body heat
production.

Inhibition of sweating.

Promotion of cutaneous vasoconstriction to reduce heat loss from the
skin.
Other body thermoreceptors are located primarily in the spinal cord,
abdominal soft tissues, and in or around the major veins in the upper
abdomen and thoracic cavity. These receptors help to regulate body
temperature differently from the skin receptors. Essentially, they detect cold
stimuli within the internal body instead of the body surface. Neuronal effector
mechanisms activated by cold stimuli are outlined in the table below.
Activated mechanisms in response to heat stimuli
↓ Heat production
Decreased activity
Anorexia
Decreased TSH release
Decreased epinephrine release
Decreased norepinephrine release
↑ Heat loss
Cutaneous vasodilation
Sweating
Behavior modification (i.e., take off clothing)
The blood vessels just below the surface of the skin dilate in response to heat
stimulation. Vasodilation is caused by inhibition of the sympathetic centers in
the
posterior
hypothalamus,
which
is
the
same
center
that
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vasoconstriction. Complete vasodilation speeds up the rate of heat transfer to
the skin by about eight-fold. Sweating is the response to increased body
temperature above the critical level of 37°C in an effort to speed up the rate
of evaporative heat loss. A 1°C increase in body temperature is enough to
cause profuse sweating to eliminate 10 times the basal rate of body heat
production. A decrease in heat production is the result of the inhibition of the
mechanisms that cause excess heat production, such as shivering and
chemical thermogenesis. Heat production and loss is further illustrated below.
Shivering
The major motor center for shivering is found in the dorsomedial area of the
posterior hypothalamus close to the wall of the third ventricle. The region is
inhibited by warmth signals from the heat center in the anterior hypothalamicpreoptic area and excited by cold signals from the skin and spinal cord. In
fact, the region is very sensitive to temperature depressions that are easily
activated when the temperature drops even a fraction of a degree below the
critical temperature level. Once activated, it relays signals that cause
shivering through bilateral tracts on the brain stem, into the lateral columns of
the spinal cord, and finally to the anterior motor neurons. These signals
increase the tone of all skeletal muscles of the body by facilitating the activity
of the anterior motor neurons. When the tone rises above a certain critical
level, shivering begins. During severe shivering, thermogenesis can increase
up to four to five times the normal.
Chemical Thermogenesis
Greater sympathetic stimulation or number of the chemical neurotransmitters
norepinephrine
and
epinephrine
in
the
circulation
can
trigger
an
instantaneously speed up cellular metabolism. This is called chemical
thermogenesis. Its occurrence is a partial result of the uncoupling of oxidative
phosphorylation by these two neurotransmitters. This means that surplus
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foodstuffs are converted and released into energy in the form of heat without
causing adenosine triphosphate (ATP) to be formed. High levels of circulating
thyroxine may also stimulate chemical thermogenesis.
Set Point for Temperature Control
The intensity of chemical thermogenesis that happens in the body is
approximately directly proportional to the amount of brown fat in the tissues.
Brown fat is heavily populated with special mitochondria, the cellular organelle
where uncoupled oxidation takes place. Brown fat also has a rich supply of
sympathetic nerves, which secrete norepinephrine, in turn triggers the
expression of thermogenin and increases thermogenesis.
Acclimatization has profound effects to the degree of chemical thermogenesis.
For example, a rat that has been exposed to a cold environment for long
periods show a 100 to 500 percent increase in thermogenesis when severely
exposed to cold. In contrast, a rat that is unacclimatized and exposed to the
same cold stimuli responds with only one-third increase in thermogenesis.
Consequently, the animal also experiences an increase in food intake. Adult
humans, on the other hand, have almost no brown fat. Therefore, it is
exceptionally uncommon for chemical thermogenesis to speed up the rate of
heat production more than 10 to 15 percent. However, infants have a small
amount of brown fat in the interscapular space. Because of this, chemical
thermogenesis can speed up heat production to as much as 100 percent. This
is a significant factor in keeping normal body temperature in neonates.
Effects of Thyroxine Output on Heat Production
As mentioned previously, thermogenesis is triggered by the presence of cool
stimuli. A cool stimulus stimulates activity within the anterior hypothalamus,
increasing the production of the metabolic hormone thyrotropin-releasing
hormone
(TRH)
in
the
region.
Once
produced
and
released
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the
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hypothalamus, it is transported to the anterior pituitary gland via the
hypothalamic portal veins. There, the hormone stimulates the secretion of
thyroid-stimulating hormone (TSH), which speeds up cellular metabolic
activity.
Thyroid-stimulating hormone (TSH) speeds up metabolic activity by increasing
the thyroxine secretion by the thyroid gland. The large number of circulating
thyroxine activates uncoupling protein and speeds up metabolism in all cells of
the body. This mechanism is also called chemical thermogenesis. However,
the increase in cellular metabolic activity does not happen instantaneously,
rather, it requires long periods of exposure to cold. Usually, several weeks of
exposure to cold stimuli results in thyroid gland hypertrophy, allowing for
greater secretion of the thyroxine hormone. However, since humans have the
natural instinct to avoid this degree of cold exposure, the quantitative extent
to which the increase in the thyroid gland size contributes to the human
adaptation to cold remains uncertain. Other animals that are exposed to
extreme cold for several weeks also experience a 20-40 percent hypertrophy
of their thyroid glands.
Studies
have
found
that
military
personnel assigned to the Arctic for a
period
of
several
months
develop
increased metabolic rates. Inuit-Yupik
(Eskimos) have also been found to have
unusually elevated basal metabolic rates.
Additionally, it is believed that the effects
of
constant
cold
stimulation
to
the
thyroid gland are partially responsible for
the greater frequency of toxic thyroid
goiters in such individuals and others
who reside in cold climates.
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As explained previously, a body core temperature of above or below 37.1°C
can result in severe alterations to the thermoregulatory mechanisms, affecting
both heat loss and heat production. Temperatures above this level result in
rapid heat loss that is greater than heat production, which eventually leads to
its decline until it reaches the set point again. Alternatively, temperatures
below this level result in rapid heat production that is greater than that of
heat loss, which eventually leads to its elevation until it reaches the set point
again. Ultimately, the thermoregulatory mechanisms in the body continually
attempt to bring the body core temperature back to this set-point level.
Feedback Gain
Feedback gain is used to measure the effectiveness of the thermoregulatory
system. It is crucial for the internal core temperature to remain constant at all
times amid fluctuations in the temperature of the external environment. The
feedback gain of the thermoregulatory system is equal to the ratio of the
change in environmental temperature to the change in body core temperature
minus 1.0. The formula for feedback gain is given below:
Feedback gain = ∆ environmental temperature -1
∆ body core temperature
Results of experiments involving humans show that body temperature
changes about 1°C for every 25-30°C change in the temperature of the
external environment.
Effects of Internal Temperature
The temperature set point in the hypothalamus is determined mainly by the
intensity of activity of the heat thermoreceptors in the anterior hypothalamus.
However, temperature signals from other parts of the body, such as the skin
and spinal cord tissues and abdominal viscera also contribute partially to body
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temperature regulation by altering the set point of the hypothalamic
thermoregulation center. The set point increases as the skin temperature
decreases. This means that when the skin temperature is high, sweating
begins at a lower hypothalamic temperature compared to when the skin
temperature is low. This is especially important to prevent excessive loss of
body heat. A similar effect happens in shivering. When the skin encounters
cold stimuli, the hypothalamic centers are activated towards the shivering
threshold even when the hypothalamic temperature may be normal. This is
especially important because a cold skin temperature can result in severely
depressed body temperature unless heat production is increased.
Local Cutaneous Temperature Reflexes
When an individual puts a foot under a hot lamp and leaves it there for a few
minutes, local capillaries dilate and mild local sweating occurs. Alternatively,
when a foot is placed in cold water, local vasoconstriction and local cessation
of sweating occur. Both reactions are caused by local effects of temperature
changes directly on the blood vessels and also by local cord reflexes that run
from skin receptors to the spinal cord and back to the same skin cutaneous
region and the sweat glands. The intensity of these local effects is, in addition,
controlled by the central brain temperature controller, so their overall effect is
proportional to the hypothalamic heat control signal times the local signal.
Such reflexes can help prevent excessive heat exchange from locally cooled or
heated portions of the body.
Behavioral Modification
Aside from the autonomic mechanisms in thermoregulation, the body can also
control body temperature through behavioral modification. When the internal
body temperature increases significantly, signals from the anterior and
posterior hypothalamus sends out a psychic sensation of overheat. On the
other hand, when the body temperature drops too low, signals from the skin
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and visceral tissue receptors draw out the feeling of cold discomfort.
Consequently, the individual makes proper environmental adjustments to
restore comfort, such as building a fire, turning on the heater, or putting on
warmer clothing in cold weather. This voluntary behavior modification is a
powerful mechanism of thermoregulation that most physiologists believe to be
an evolved human survival response. In fact, this is the only effective
mechanism that retains body heat in extremely cold environments.
Classification of Hypothermia
Hypothermia is defined as a core body temperature below 35°C. Traditionally,
it’s been classified as discussed below:1

Mild hypothermia: a body core temperature between 32-35°C,

Moderate hypothermia: a body core temperature between 28-32°C, and

Severe hypothermia: a body core temperature below 28°C.
Mild Hypothermia
When the core temperature drops by 0.7°C, mild hypothermia ensues and is
manifested by shivering. It also results in the increase of the metabolic rate
by up to 5 times. When the core temperature drops down further to 32°C, the
individual may shiver uncontrollably. The severe fall of core temperature also
produces cutaneous vasoconstriction, tachycardia, greater cardiac output,
increased
plasma
catecholamine
levels,
cold-induced
diuresis
and
hyperglycemia. If glycogen stores in the liver are exhausted, hypoglycemia
may occur which inhibits shivering. In addition, the plasma levels of
thyrotropin releasing hormone (TRH), triiodothyronine (T3), L-thyroxine (T4),
growth hormone, thyroid-stimulating hormone (TSH) and adrenocorticotropic
hormone (ACTH) stimulation tests remain normal, all of which indicate a
normal pituitary, adrenal and thyroid function during mild hypothermia.
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Moderate Hypothermia
When the core temperature drops below 33°C, shivering slowly diminishes,
replaced by stiff muscles and joints and a delayed relaxation phase of the
stretch reflexes. If left untreated, the individual exhibits signs of lethargy and
drowsiness. Unconsciousness rarely happens at temperatures greater than
28°C, which is why other potential causes of coma should be investigated if
coma exists. The pulse, blood pressure and respiratory rate are usually
low.
Severe Hypothermia
When the core temperature falls below 30°C, the individual becomes
poikilothermic and it is unable to spontaneously return to the set point. In
these cases, active re-warming must be initiated. At temperatures below
28°C, the patient loses consciousness and reflexes, and there is a faint pulse.
The patient may also exhibit with fixed and dilated pupils.
Bradycardia and atrial fibrillation occur at temperatures below 30°C and
ventricular fibrillation can occur at temperatures below 28°C. At 20°C,
asystole is seen more than ventricular fibrillation. Respiratory depression may
occur along with bronchorrhea. Pulmonary edema is uncommon. Circulatory
arrests for 10 minutes at 30°C, 25 minutes at 25°C, 45 minutes at 20°C and
60 minutes at 16°C are the frequently used limits for cerebral function to
return to normal; although, studies suggest that these limits can go higher.
Outlined in the table below is the summary of the traditional classification of
hypothermia and their characteristic clinical findings and vital signs.
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Degree of
Core Temperature
Clinical Findings and Vital Signs
Hypothermia
Uncontrolled shivering
Mild
32°C to 35°C
Cold-induced diuresis
Hyperglycemia
Tachycardia
Diminished shivering
Moderate
28°C to 32°C
Stiff muscles and joints
Slow stretch reflexes
Lethargy and drowsiness
Unconsciousness
Ventricular and atrial fibrillation
Lost reflexes
Severe
-28°C
Fixed and dilated pupils
Bradycardia
Asystole
Respiratory depression
Bronchorrhea
The classification of hypothermia has recently been revised using the Swiss
staging system. Its classification is based on vital signs. Outlined in the table
below is the Swiss staging system of hypothermia and their corresponding
clinical findings and vital signs.
Staging
Core Temperature Range
Clinical Findings and Vital Signs
HT I
35°C to 32°C
HTII
<32°C to 28°C
Impaired consciousness, not shivering
HT III
<28°C to 24°C
Unconsciousness, not shivering, vital signs
Conscious, shivering
present
HT IV
<24°C
No vital signs
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Mechanism of Environmental Heat Loss
As mentioned previously, cellular metabolism is primarily responsible for heat
generation. The metabolism of food and water, muscular activity, and
biological chemical reactions all contribute to thermogenesis. Environmental
heat loss occurs via several different mechanisms, which include:

Radiation:
Radiation accounts for more than 50 percent of heat loss. It occurs
under dry conditions. A good example of heat loss through radiation is
the dissipation of up to 50 percent of the body’s heat through an
uncovered head.

Conduction:
Conduction accounts for about 15 percent of heat loss. The direct
transfer of heat to a nearby object that is cooler than the body is a very
common cause of accidental hypothermia. The heat lost is only a small
fraction but wet clothing causes a twenty-fold increase in heat loss.
Conversely, submersion in cold water increases heat loss by as much as
thirty-fold. In fact, conduction is an important mechanism of heat loss in
drowning or immersion accidents.

Convection:
Convection also accounts for approximately 15 percent of heat loss. The
heat transfer occurs when the air movement creates loss of the warm
layer of heat near the body; and, the degree of heat loss is dependent
on the speed of the wind. A good example is a wind traveling 12 mph,
which increases heat loss by as much as five-fold.
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
Evaporation:
Evaporation accounts for approximately 20 percent of heat loss. Heat is
lost when liquids are converted into gas. One good example is sweating
and respiration wherein the consequent evaporation of water will cool
the body at the rate of 0.6 kcal per gram.
Hypothermia also causes cellular membrane disruption, allowing intracellular
fluid to leak out, and enzymes to start malfunctioning. Consequently,
electrolyte imbalance occurs, particularly hyperkalemia. The intra- and
extracellular water begins to crystallize resulting in cellular death, if not
alleviated in time. During hypothermia, the hypothalamus tries to stimulate
thermogenesis
through
shivering
and
chemical
means
(i.e.,
increase
catecholamine secretion and adrenal activity). To minimize heat loss, blood
flow to the peripheral tissues is reduced through vasoconstriction.
Hypothermia has profound effects on almost all organ systems. These effects
are particularly significant in the cardiovascular system and the central
nervous system (discussed later in the course). Hypothermia results in
reduced depolarization of cardiac pacemaker cells, resulting in bradycardia.
Because the vagal nerve does not mediate it, this form of bradycardia can be
refractory to standard therapies such as atropine. In addition, mean arterial
pressure and cardiac output decline, and an electrocardiogram may exhibit
the characteristic J or Osborne waves. Although the wave is especially seen in
hypothermic individuals, it may be a normal variant as seen sometimes in
sepsis and myocardial ischemia.
Causes And Risk Factors Of Hypothermia
The external environment presents with several precipitating factors such as
an acute exposure to cold in an otherwise previously fit individual, a relatively
brief exposure to mild cold during an ongoing illness such as sepsis, or
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inactivity after a fall. A previously fit and young individual with hypothermia
generally has a good prognosis in the absence of circulatory arrest. Factors
and predisposing causes mentioned in preceding sections are outlined in the
table below and discussed in more detail here.1-5
FACTORS
EXAMPLES
Environment
Time of the year
Ambient temperature
Wind chill
Water chill
Humidity
Behavior
Inadequate or wet clothing
Immersion
Prolonged exposure
Fatigue
Lack of physical fitness
Inadequate shelter and heat
Drugs
Alcohol
Nicotine
Opiates
Barbiturates
Benzodiazepines
Tricyclic antidepressants
Phenothiazines
Impaired hypothalamic thermoregulation
Very old age
CNS trauma
Stroke
Wernicke’s encephalopathy
Burns
Sepsis
Acute myocardial infarction
Chronic renal failure
Neoplasms
Pancreatitis
Decreased heat production
Hypothyroidism
Hypoglycemia
Anorexia
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Adrenal insufficiency
Hypopituitarism
Older age
Reduced lean body mass
Impaired mobility
Reduced shivering mechanism
Inadequate diet
Comorbidities
such
as
sepsis,
diabetes
mellitus
In a study of 85 consecutive hypothermic patients at San Francisco General
Hospital, it was found that a coexisting infection was the primary cause in 33
of them, and alcohol ingestion in 27 of them. In fact, environmental exposure
accounted for only 9 cases. About 50 percent of these hypothermic patients
died. As already mentioned, hypothermia is a failure of thermoregulatory
control. Several factors and predisposing causes are attributed to its
development including the external environment, old age, acute and chronic
diseases and disorders, and pharmacological agents.
Decreased Heat Production
Endocrine dysfunctions are known causes of decreased heat production. These
include hypopituitarism, adrenal insufficiency, and hypothyroidism. These
endocrine
disorders
must
be
considered
in
patients
presenting
with
unexplained hypothermia who fail to rewarm with conventional treatment
modalities. Other causes may also play a role such as severe anorexia,
hypoglycemia and neuromuscular degenerative disorders such as Parkinson’s
disease.
Increased Heat Loss
Increased heat loss can result from behavioral, iatrogenic, and other etiologic
factors. These factors contribute to the severity of accidental hypothermia
caused by immersion and non-immersion etiologies. Both these types of
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hypothermia are the two most commonly encountered in the emergency
department.
Skin disorders and injuries such as psoriasis and burns decrease the body's
ability to preserve heat. Cold infusions, rapid treatment of heat stroke, and
emergency deliveries can all cause hypothermia due to increased heat loss.
Drugs as a Cause of Heat Loss
Drugs can also facilitate heat loss by causing thermoregulatory failure.
Patients who are on opioids and psychotropic drugs may present with induced
vasodilatation. Alcohol and phenothiazines decrease the body’s ability to
respond to low ambient temperatures. Alcohol is especially dangerous because
it not only changes the perception to cold and impairs judgment, but also
causes peripheral vasodilation that boost the loss of heat. Alcohol can also
cause impaired shivering and hypoglycemia. In addition, it can also lower the
core temperature by exerting direct effects on the hypothalamus.
Phenothiazines can cause central thermoregulation dysfunction and inhibition
of peripheral vasoconstriction in response to cold through their blockade of
alpha-receptors. Other alpha-blockers such as prazosin have also been
reported to cause hypothermia, with the elderly being more susceptible to
their alpha blocking activity.
Lithium overdose and valproic acid at therapeutic doses have been reported to
cause a drop in core temperature.
Impaired Hypothalamic Thermoregulation
Disorders affecting the hypothalamus can impair its ability to perform its
thermoregulatory function. Examples include central nervous system (CNS)
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trauma,
strokes,
toxicologic
and
metabolic
derangements,
intracranial
bleeding, CNS tumors, Wernicke’s encephalopathy, and multiple sclerosis.
Older Age
Older aged people are especially more prone to accidental hypothermia of
progressively impaired thermoregulatory function. The elderly usually have
decreased ability to produce heat due to decreased lean body mass, impaired
mobility, inadequate diet, and reduced shivering mechanism.
As mentioned previously, sympathetically activated thermogenesis in brown
adipose tissue only occurs among infants, not the elderly. In fact, older adults
have very little, if at all, brown adipose tissue. Additionally, the elderly are
more likely to sustain heat loss because of their impaired ability to:

Vasoconstrict properly

Discriminate changes in temperature

Adapt normal behavioral responses to cold
The elderly also have greater exposure to cold through falls or comorbidities.
This is especially true for those who have predisposing socioeconomic factors.
In fact, some elderly people are more likely to experience recurring
hypothermia, which may suggest that they may have a specific predisposition
to thermoregulatory failure that may be precipitated by a relatively minor
insult. Among the elderly, the most common precipitating factor is sepsis
brought on by severe and unresolved infection. In fact, a study found that
approximately 80% of elderly patients with hypothermia have a comorbid
systemic infection.
Sepsis predisposes the elderly to hypothermia by either of the following:

Causing vasoconstriction failure
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
Inducing an abnormal hypothalamic response. The mechanism by which
it stimulates an abnormal hypothalamic response remains unclear;
however,
study
reports
have
found
an
abnormally
increased
inflammatory response, with elevated levels of tumor necrosis factor
alpha (TNF‐α) and interleukin‐6, and increased prostacyclin and
thromboxane B2 metabolites.
Inflammation of the pancreas and diabetic ketoacidosis are also precipitating
factors that can cause hypothermic episodes, even if they are not clinically
noticeable.
This
is
especially
true
for
people
with
diabetes
and
malnutrition.
Complications And Related Dysfunctions
Mild hypothermia usually does not cause any permanent damage. People with
mild hypothermia usually recover easily. However, people with moderatesevere hypothermia may suffer from serious complications and even death.
Children
have
greater
chances
of
recovery
from severe
hypothermia
compared to adults. In fact, the death rate for hypothermia in the elderly is
about fifty times more than in children. The following discussion highlights
complicating and other related factors or dysfunctions occurring during
exposure to freezing conditions and resulting hypothermia.1-3,5,6
Complications
There are several possible complications from hypothermia, classified as
mental and physical. The mental complications include paradoxical undressing
and terminal burrowing. Physical complications include frostbite, frostnip,
trench foot, and chilblains.
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Mental Complications
The mental complications are the so-called paradox reactions of hypothermia
by victims prior to their deaths. Paradoxical undressing is a dangerous state of
hypothermia and occurs before terminal burrowing. It is a term used to
describe the final undressed state of the victims of hypothermia. Just before
death, they remove all their clothes (as if burning up), in an effort to cool
down despite their severely hypothermic state. Consequently, they are often
found naked and frozen to death. The reason for this paradoxical reaction may
be due to the cold-paralysis effect of the nerves in the blood vessels, leading
to reflexive vasodilation, which in turn results in the false sense of warmth.
Another theory suggests that the reflex vasoconstriction that occurs during
the first stage of hypothermia cause paralysis of the vasomotor center, also
leading to a false sense of warmth despite the lethal hypothermic state of the
body.
Terminal burrowing occurs after these victims have undressed. This type of
behavior refers to their attempts at crawling into small and enclosed spaces.
This is why victims of lethal hypothermia are not only often found naked; they
are often huddled and squeezed into cupboards and shelves, garbage cans,
underneath beds, and behind wardrobes. The discovery positions of their
bodies are akin to protective burrowing-like or hiding-like behaviors.9
The clothes of the victims are almost always scattered on the ground in front
of their final position, suggesting the occurrence of paradoxical undressing
before terminal burrowing. Also, these victims are often found with abrasions
and hematomas on their knees, elbows, feet and hand, suggesting movement
on
all
fours
(crawling)
after
undressing
and
just
before
terminal
burrowing.
In 1995, an article published in the International Journal of Legal Medicine
told the story of German researchers who studied and described hypothermia
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victims in a position which indicated a final mechanism of protection. Although
terminal burrowing is a behavior that isn’t understood well by the scientific
community, the German researchers described it as an autonomous process
of the brain stem, triggered in the final state of hypothermia; it produces a
primitive and protective burrowing-like behavior akin to conduct found in
hibernating animals.
Physical Complications
Frostbite and Frostnip
Frostbite is a term used to refer to local tissue (nerves, muscles, blood
vessels) damage and injury due to severely cold temperatures. Frostnip is a
mild degree of frostbite and usually only involves the surface of the skin. It is
characterized by tingling sensations and numbness due to severely cold
temperatures.
Frostbite generally affects the tissue extremities, with the hands and feet
being the most common sites of tissue damage and injury. Other extremities
vulnerable to frostbites are the ears, nose, cheeks, and penis. Because
hypothermia affects the elderly and pediatric populations more than any other
population group, it stands to reason that they are also the group most
susceptible to frostbites and frostnips. However, frostbite is also fairly
common in adults between 30-50 years of age.
Numerous studies from the Scandinavian countries found that frostbite is
frequently linked with wet and improper winter clothing, history of previous
hypothermia or frostbite, wound infections, diabetes, and smoking. These
factors are also frequently seen in homeless individuals necessitating health
authorities to be vigilant for frostbite during the cold weather.
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Trench Foot
Trench foot is also known as immersion foot. The term refers to an injury of
the feet due to prolonged exposure to wet and cold terrains. It can happen at
temperatures as high as 16°C given the feet are continuously exposed to a
wet environment.
This happens because wet feet lose heat 25-times faster than dry feet. In
response to that, the body attempts to inhibit peripheral blood circulation in
the feet by constricting their blood vessels in order to preserve heat and avoid
its loss. Consequently, the skin tissue undergoes necrosis due to lack of
oxygen and nutrients and accumulation of toxic products.
Chilblains
Chilblains refer to capillary injuries to the cheeks, ears, fingers and toes due
to their repeated exposure to temperatures as high as 16°C. The cold
exposure permanently injures the capillary beds in the skin. The redness and
itching are usually felt with additional exposure.
The signs and symptoms of all four physical complications are summarized in
the table below.
Frostbite/Frostnip
Trench foot
Chilblains
Fingers/toes reduced blood flow
Reddening of the skin
Redness
Numbness
Numbness
Itching
Tingling sensations
Leg cramps
Possible blistering
Aching or stinging sensations
Swelling
Inflammation
Bluish, waxy skin
Tingling pain
Possible ulceration (severe case)
Blisters or ulcers
Bleeding under skin
Gangrene
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Mechanism of Injury in Frostbites
There are three processes that occur simultaneously in frostbites, and these
include the following.
1. The freezing of the tissue is accompanied by the formation of ice
crystals that damage the cell membranes. Water then leaks out of the
cells, leading to cellular dehydration and death.
2. Peripheral blood vessels constrict in response to the cold, depriving the
tissue of oxygen. The flow of blood in the capillaries ceases, leading to
clotting or thrombosis within small arterioles and venules. This further
exacerbates the hypoxia in the tissue.
3. Inflammatory mediators are released in response to all of these insults:
local tissue damage, hypoxia, and thrombosis. The most potent are the
prostaglandins
PGF2
and thromboxane
A2.
These cause
further
vasoconstriction, depriving the tissue of yet more oxygen, and also
cause platelet aggregation, exacerbating the thrombosis. The peak time
for the release of these mediators is during the rewarming process.
The goal of treatment is to reverse or limit each of these processes.
Rewarming can stop the tissue from freezing and reverse the vasoconstriction,
while medications can block the release of the inflammatory mediators.
Related Dysfunctions
Other complications of hypothermia include renal, metabolic, cardiovascular,
hematologic, neuromuscular, respiratory, and gastrointestinal dysfunctions.
Each one is discussed in detail below.
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Renal and Metabolic Dysfunctions
As
mentioned
previously,
a
mild
decline
in
body
temperature
(mild
hypothermia) can result in a cold-induced diuresis. This is originally caused by
the enhanced renal blood flow following vasoconstriction, then with declining
temperature, the decrease in distal tubular reabsorption of water and the
resistance to the effects of the anti-diuretic hormone (ADH). The cold-induced
diuresis occurs together with enhanced urinary electrolyte excretion, which
may be attributed to decreased tubular sodium reabsorption.
In moderate hypothermia, the glomerular filtration rate (GFR) declines
together with cardiac output, resulting in declining renal blood flow by as
much as half at temperatures between 27–30 °C. In addition, this is
accompanied by declining tubular function and renal clearance of glucose.
When the core temperature falls below 27°C, the tubular capacity for
hydrogen ion secretion decreases, thus, further aggravating the acidosis. In
the clinical setting, acute renal failure is seen in more than forty percent of
patients with accidental hypothermia who were admitted to the intensive care
unit. Tissue examination has revealed ischemic damage to the kidneys, which
may have occurred during the rewarming phase, after a period of relative
protection at lower temperatures.
Total body metabolism declines in response to worsening hypothermia, as
measured by a decline in oxygen consumption, which is about six percent for
every degree Celsius fall in temperature. Consequently, the basal metabolic
rate declines by 50% at 28 °C. Conversely, pituitary, adrenal and thyroid
functions remain normal. However, some researchers have observed a
depressed
cortisol
response
to
stimulation
of
the
adrenocorticotropic
hormone. Although TSH and thyroxine plasma concentrations tend to remain
at normal levels, they should still be assessed in order to rule out
hypothyroidism as an underlying cause.
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Hypothermia can also cause hyperglycemia. Elevated corticosteroid levels,
accompanied by direct cooling of the islets of Langerhans, repress the release
of insulin release and impair insulin uptake at the peripheral tissues. There is
also an increase in sympathetic activity, accompanied by elevated plasma
norepinephrine and free fatty acid concentrations. Due to the elevated levels
of catecholamine, glycogenolysis and gluconeogenesis ensues contributing to
the hyperglycemia. Likewise, glucagon concentrations rise. The plasma
cortisol concentrations correspond to lactate and glycerol concentrations,
suggesting an active stimulation of glycogenolysis and lipolysis.
In situations where hypothermia has progressed gradually or chronically,
glycogen reserves may be exhausted, and leading to greater likelihood of the
development of hypoglycemia. Shivering may also contribute to the depletion
of glycogen reserves and chronically contribute to hypoglycemia. Hypokalemia is caused by the movement of extracellular potassium into the
cells, stimulated by alterations in cell membrane permeability and the activity
of the sodium-potassium pump. Conversely, hyperkalemia indicates acidosis
and necrosis, all of which are signs of poor prognosis.
Cardiovascular Dysfunctions
In cases of mild hypothermia, tachycardia and peripheral vasoconstriction is
seen initially followed by an increase in cardiac output and slight increase in
blood pressure. Moving onto situations of moderate hypothermia, bradycardia
ensues as a result of reduced spontaneous depolarization of the pacemaker
cells. An increase in systemic vascular resistance brought on by autonomic
reflex response and catecholamine secretion can balance the reduced cardiac
output. Additionally, the increase in systemic resistance may be attributed to
hemoconcentration, greater viscosity and local vasomotor responses.
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Osborn or J-waves on the electrocardiogram are evidence of repolarization
abnormalities in hypothermic patients. The waves increase proportionally in
amplitude with declining temperature, but remain unaffected by electrolyte
disturbances. It must be remembered though that J waves are not exclusively
seen in hypothermia; they are also present in patients who sustained
myocardial ischemia, subarachnoid hemorrhage and other head injuries.
Hence, they are not diagnostic for hypothermia.
Additionally, broad QRS complexes also develop, suggesting a slower pace of
myocardial electroconduction. This is usually accompanied by notable ECG
changes such as elevated or depressed ST-waves and inversed T-waves, all of
which
may
be
attributed
to
the
developing
acidosis.
The
slowed
electroconduction of the myocardial muscles may be attributed to decreased
and late activation of the inward sodium current. There is also greater PR
interval and second or third degree atrioventricular block suggesting a
prolongation of systole, and conduction delay. QT prolongation may appear at
lower temperatures and is evidenced by delayed repolarization.
At a temperature of 28°C, the heart rate drops to 30–40 beats per minute. At
even lower temperatures (i.e., 20°C), the bradycardia may worsen, with rates
falling dangerously low to 10 beats per minute. Systemic vascular resistance
reduces
as
catecholamine
release
and
cardiac
output
decreases.
At
temperatures below 24°C, the risk of asystole increases. There have been
suggestions that asystole is a primary symptom of hypothermia, whereas
ventricular fibrillation develops secondary to re-warming, hypocapnia, or
alkalosis.
Ischemia, amplified adrenergic activity and electrolyte imbalance help lead to
myocardial instability such as arrhythmias in cases of moderate hypothermia.
Ventricular fibrillation is frequently seen at temperatures below 27°C. Its
likelihood of occurrence is greater with sudden alterations, such as:
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
Physical movement

pO2 or pCO2

Myocardial temperature

Biochemical or acid/base status
Serum levels of hydroxybutyrate dehydrogenase and creatine kinase are
sometimes slightly greater than normal, but may not necessarily suggest
cold-induced ischemic myocardial damage. This is because creatine kinase
serum levels rise independent of temperature, and do not occur with
concurrent ECG changes or histological proof of myocardial infarction at
postmortem exams. Another, more reliable marker of cardiac damage is
troponin measurements.
Hematologic Dysfunctions
Hypothermia cause hematological disturbances such as increases in:

Blood viscosity

Fibrinogen

Hematocrit
These disorders are the primary underlying cause of many of the dysfunctions
of other organs. Altered vascular permeability leads to loss of plasma to
extravascular
compartments,
resulting
in
hemoconcentration,
and
consequently, worsened hypovolemia (due to cold-induced diuresis). A 2%
increase in hematocrit levels is seen for every 1°C decline in temperature.
However, a normal hematocrit level in moderate or severe hypothermia is
suggestive of pre-existing anemia or hemorrhage. In addition, hypothermia
has also been found to be associated with marrow suppression and
progressive marrow failure, and induction of erythroid hypoplasia and
sideroblastic anemia.
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Cold stimuli directly prevent the enzymatic reactions in the intrinsic and
extrinsic pathways of the clotting cascade, leading to a coagulopathy. The
prothrombin time and partial thromboplastin time may remain normal when
the measurements are taken at 37°C, but, may significantly increase if
measured at lower temperatures, even with normal clotting factor levels.
Reports of a disseminated intravascular coagulopathy may be attributed to the
release of tissue thromboplastin from ischemic tissue, or its circulatory
collapse itself.
Hypothermia can also interfere with endothelial synthesis of prostacyclin
(PGI2) and its inhibitory action on platelet aggregation, triggering platelet
activation and thrombosis. Conversely, thrombocytopenia may also develop.
This frequently results from any of the following three causes: sequestration
in the liver and spleen, or disseminated intravascular coagulation, or bone
marrow depression. Additionally, the synthesis of thromboxane B2 by platelets
is dependent on temperature, thus, promoting a fall in platelet activity with
declining temperature.
Above normal cryofibrinogen concentrations can sometimes occur in situations
of hypothermia. This is responsible for dramatically elevating the blood
viscosity, in response to progressively cold temperatures; and, interfering
with the microcirculation and, possibly, leading to the commonly found tissue
micro-infarcts.
Greater
incidence
of
purpura
is
suggestive
of
cryofibrinogenemia, and is linked to increased mortality.
The exhaustion of leukocytes can happen due to hypothermia. It is therefore
important to consider sepsis in elderly patients with hypothermia to be a
predisposing cause of thermoregulation failure. Consequently, antibiotic
coverage should be seriously considered in this patient population.
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Neuromuscular Dysfunctions
Hypothermia causes clinically apparent central neurological effects, which are
listed below:

Initial confusion

Amnesia (mild hypothermia)

Apathy

Impaired judgment

Paradoxical undressing

Terminal burrowing

Dysarthria

Coma
Severe hypothermia (25°C) also results in loss of cerebrovascular autoregulation and reduction in cerebral blood flow by six to seven percent for
every 1°C drop in temperature. However, there is also an apparent decrease
in metabolic rate, thus, relatively increasing to cerebral ischemia. At
temperatures below 20°C, ischemic tolerance is ten times the normothermic.
This is evident in a flat electroencephalogram reading.
Shivering increases in cases of mild hypothermia but then decreases as the
temperature drops further. However, the temperature at which shivering is
lost varies greatly, from as low as 24°C to as high as 35°C. There is also an
increase in viscosity of synovial fluid at lower temperatures, which explains
the symptoms of stiff muscles and joints in moderate hypothermia.
Neurological deficits such as ataxia and loss of fine motor control develops
during the initial stages of hypothermia, then followed by hyporeflexia, and
extensor plantar response and delayed pupillary response in moderate
hypothermia.
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Rigidity, pupillary dilatation and areflexia develop when temperatures drop
below 28°C. The stiff muscles and joints may deceptively look like rigor
mortis, although the stiffness may paradoxically diminish as the temperature
declines further.
These can be explained by animal studies in peripheral nerve conduction.
There is a progressive decrease in conduction velocity with declining
temperatures, which may be attributed to a reduced movement of potassium
and chloride ions across the axon membrane. The delay in synaptic
transmission is also aggravated due to a cooled neuromuscular junction.
Muscle contraction is, to some extent, temperature-dependent; decreased
tension development and maximal shortening velocity occurs at lower
temperatures. At skin temperatures as low as 12°C, the pre-capillary
sphincters do not contract, resulting in vasodilatation and increased blood
flow. The latter may then lead to sufficient warming to restore capillary
function and restoration of local vasoconstriction. The shift between dilatation
and constriction is referred to as the Lewis Hunting Reaction and affects
primarily the peripheries such as the fingertips, toes, ears and face.
Respiratory Dysfunctions
Mild hypothermia also has several respiratory effects. For instance, in mild
hypothermia, an initial tachypnea is seen followed by decreased minute
volume and oxygen consumption, leading to bronchospasm and bronchorrhea.
In moderate hypothermia, there is a decrease in protective airway reflexes
due to impaired ciliary function, predisposing the patient to aspiration and
pneumonia.
In addition to reduced oxygen consumption, there is also a marked decrease
in carbon dioxide production by about 50 percent at 30°C. Core temperature
control is especially dependent on pCO2 level, identified by the carotid bodies,
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which in turn act on sources of heat production and thermal decomposition.
The ventilatory drive is depressed by the direct cooling effect at the
respiratory centers. At temperatures less than 34°C, there is greater
sensitivity to pCO2 stimulation despite the maintenance of the hypoxic drive to
deeper levels of hypothermia.
Physiological and anatomical respiratory dead spaces rise due to
bronchodilation, however, alveolar dead space remain normal. Hypothermia
does not affect the local gas exchange but it does cause greater pulmonary
vascular resistance and ventilation-perfusion mismatch. Severe hypothermia
causes chronic hypoventilation, apnea, and rarely, pulmonary edema.
In addition, there is an initial shift to the left of the oxyhemoglobin
dissociation curve due to declining temperature. This leads to a dysfunctional
oxygen delivery and tissue hypoxia, although this is balanced to some extent
by the consequent lactic acidosis and other respiratory and metabolic factors
causing the acidosis. Shivering can also contribute to the increase in lactate
production, and its subsequent impaired hepatic clearance.
Most often, the metabolic acidosis aggravates during re-warming efforts as
the products of anaerobic metabolism are brought back into the blood, which
can compound the risk of arrhythmias. In severe hypothermia, there is a
corresponding severe resulting in an overall shift to the right of the
oxyhemoglobin dissociation curve. The impediment to the delivery of oxygen
to the hypoxic tissues is not as significant due to the fall in oxygen
requirement at lower temperatures.
Gastrointestinal Dysfunctions
Intestinal movement is compromised at temperatures less than 34°C, leading
to ileus when the temperature falls even further at less than 28°C. There may
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also be punctate hemorrhages seen all over the GI tract. In addition, it is not
uncommon for gastric erosions and submucosal hemorrhages to occur,
although they are not clinically significant. The superficial gastric ulcers called
Wischnevsky's ulcers are found in many cases during autopsy investigations.
A characteristic linear pattern is usually present which is commonly found in
patients who succumbed to acute cold stress.
In addition, liver function is affected, possibly due to decreased blood flow
brought on by reduced cardiac output. Consequently, the metabolic clearance
of lactic acid is reduced contributing to the existing acidosis. The pancreas is
also affected by hypothermia. Its resulting inflammation is found during
postmortem exams in more than one-fourth of cases. There is also a mild
increase in serum amylase in the absence of clinical evidence of pancreatitis in
half of the patients studied. There is no clear explanation for this but studies
suggest that it is due to the thrombosis in the microcirculation, and
consequent ischemia and perilobular necrosis in the organ. Some studies
thought this occurrence share a similar underlying process to that which
causes tiny infarcts in the stomach, liver, brain, myocardium, and many other
organs. Portal vein thrombosis may also be seen together with hemorrhagic
pancreatitis.
Assessment And Treatment Of The Hypothermic Patient
There are several factors to consider when assessing patients suspected of
hypothermia. These include: 1) A history of cold exposure, 2) A history of
predisposing disease, 3) Presence of a cold trunk, and 4) Core body
temperature below 35°C. As mentioned previously, hypothermia can be
staged clinically on the basis of vital signs. This is preferred over the
traditional staging system in cases when the core temperature cannot be
accurately measured. The following discussion details aspects of assessing
and treating a hypothermic patient.5,7-13
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Accurate Temperature Determination
Core temperature measurement is required to confirm staging of hypothermia
and consequently, help emergency responders arrange for appropriate
transport and management decisions. In order to get an accurate reading,
properly calibrated, low-reading thermometers must be used, although these
may not always available in the pre-hospital setting. As mentioned previously,
body temperature varies between body sites, present degree of perfusion, and
temperature of the surrounding environment.
A thermistor probe inserted into the lower third of the esophagus is preferably
used to obtain the core temperature in patients who are intubated. There is a
risk of obtaining a falsely elevated temperature if the probe is inserted
proximally, due to its exposure to warmed gases. The temperature obtained
by a probe in touch with the tympanic membrane is an accurate reflection of
the brain temperature, given the ear canal is not contaminated with snow and
cerumen, and shielded from the cold environment.
Caution should be taken when using IR cutaneous, aural, bladder, rectal and
oral thermometers to measure core temperatures since these often offer
inaccurate readings in patients with hypothermia. The bladder temperature
can rise during diagnostic peritoneal aspiration (DPA). Thermistor probes
measuring rectal temperatures should be inserted into a depth of 150 mm.
However, these readings may reflect a delayed core temperature during
rewarming.
It is important to remember that a reliably accurate measurement is not
always feasible, such as occurs in various field settings. Initial rescue and prehospital treatment decisions should be based on the current Swiss staging
system of hypothermia.
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Physical Examination
The physical examination of hypothermic patients is challenging, especially in
moderate to severe hypothermia. These patients can appear dead or
comatose, with very faint and hard-to-hear blood pressure, shallow to absent
respirations, non-palpable pulse, dilated pupils, absent deep tendon reflexes,
and increased muscle tone deceptively similar to rigor mortis.
Assessing the core temperature of hypothermic patients requires nurses and
emergency responders to basically look, listen and feel for vital signs and
other clues that can help guide management decisions. They may find it
useful to follow the steps outlined below in assessing patients who are
conscious and able to talk.
1. Look at the patient, talk and ask questions when assessing the airway.
Listen for sounds of noisy breathing since it is a strong indication for
airway obstruction.
2. Gather as much information as to how they are feeling. Some patients
may feel shivery, and sometimes hot, and then cold. This subjective
information actually gives clues to changes in core temperature of the
patients.
3. Observe the skin color. Determine whether it is pale, cyanosed, pink or
flushed. Determine the skin integrity, whether it is intact, bruised or
burnt.
4. Touch the skin and feel its temperature. Determine whether it is hot to
touch, sweaty or clammy. A skin that’s hot to touch is suggestive of
infection or dehydration.
5. Assess circulation by looking at the skin color again. Also, perform
capillary refill time (CRT) and look manually for the pulse.
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Laboratory Testing
White Blood Cell (WBC) Count
Hypothermia can affect the white blood cell (WBC) count. A rise in WBC count
in hypothermia may be attributed to leukocyte demargination, which happens
during shivering. Conversely, reduction in WBC count in hypothermia may be
due to splenic sequestration during the physiologic stress.
Hemoglobin Count
The hemoglobin and hematocrit levels may rise as a result of
hemoconcentration secondary to cold diuresis (increased urine production on
exposure to cold).
Electrolyte Concentrations
Electrolyte concentrations are altered often during re-warming efforts. The
most affected electrolyte is potassium; with levels fluctuating frequently in
response to alterations in the acid-base balance. Mild hypothermia can cause
hypokalemia, while severe hypothermia can trigger hyperkalemia secondary
to hypoxic and traumatic cell death. In fact, severe hyperkalemia is associated
with non-survival and is considered a strong indicator of hypoxia before
cooling. The greatest recorded concentrations of serum potassium in victims
of accidental hypothermia who were successfully revived are: 11.8 mmol per
liter in a 31-month-old child, 9.5 mmol per liter in a 13-year-old child, 7.9
mmol per liter in a 34-year-old adult, and 6.4 mmol per liter (in an adult who
survived burial in an avalanche).
Other electrolytes such as sodium, magnesium, calcium, and chloride levels
are not affected significantly. However, sodium levels may become elevated at
the onset of coexisting dehydration. Consequently, serum osmolality may also
rise. Studies have found that almost half of all patients admitted into the ICU
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for hypothermia have an abnormal renal function. In addition, creatine kinase
levels must be measured to assess or rule out renal failure secondary to
rhabdomyolysis or acute tubular necrosis. This is especially important in
hypothermic patients who are unconscious and do not have a medical history
on file. Lastly, hypothermic patients present with abnormal liver function tests
and decreased lactic acid elimination because of reduced cardiac output.
Microbiological Tests
Blood cultures are performed, as septicemia is a common cause of
hypothermia, particularly in the cirrhotic patient. Depending on the clinical
circumstance, urine, sputum, cerebrospinal fluid and ascitic fluid may also be
taken for culture.
Blood Gas Analysis
The blood gas values of hypothermic patients are hard to interpret and its
method of assessment is controversial. Blood gas analyzers heat the blood
sample to 37°C which results in the elevation of partial pressure of the gases
tested. The elevated pressure increases the hydrogen ion concentration of the
sample. The result of the analysis is a corrected value with deceptively
elevated CO2 levels and decreased pH levels. As a result, some hospitals and
medical practitioners prefer to use uncorrected arterial blood gas values to
direct clinical management decisions. The correction of an impaired acid-base
balance based on corrected arterial blood gas values can potentially aggravate
an existing acidosis and worsen overall prognosis by interfering with both
cerebral and coronary circulation, and potentiating arrhythmic disorders.
Hypothermic patients are especially prone to acid-base disorders. Examples of
these include:

Metabolic acidosis due to lactate

Respiratory alkalosis from the cold blood
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
Respiratory acidosis from the hypoventilation

A combination of the metabolic acidosis, respiratory alkalosis, and
respiratory acidosis
Thus, there is greater preference for directly treating the actual uncorrected
ABG, with a goal of an uncorrected pH of 7.35 and a pCO2 of 40 mm Hg.
Coagulation Studies
Severely hypothermic patients may also have severely impaired clotting
functions because clotting enzymes are temperature dependent. A study by
Rohrer
et
al.
showed
that
both
prothrombin
time
(PT)
and
partial
thromboplastin time (PTT) rise in response to temperature reduction. Fifteen
samples of pooled plasma were investigated at varying temperatures, 37°C,
34°C, 31°C, and 28°C, and showed a statistically significant elevation in both
the PT and PTT (p< 0.001) in response to declining temperatures. The mean
prothrombin time at 37°C was 11.8 seconds compared to a mean of 16.6
seconds at 28°C.
Another comparable study by Felfernig, et al., investigated the partial
thromboplastin time of in vitro plasma and found a 10 percent rise in plasma
less than 35°C compared to plasma at 37°C. In this study, the obtained
values were normal since the blood was heated to 37°C before analysis. The
results of these studies imply that both values must be considered in severely
hemorrhaging trauma patients despite seemingly normal coagulation values.
Impaired
coagulation
is
self-limiting
and
eventually
resolves
with
rewarming.
Alcohol Intoxication Level
Usually, patients presenting with altered mental status are tested for blood
alcohol levels, particularly if they are also hypothermic. This is because both
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alcohol and drug intoxication are causative and aggravating factors to
hypothermia. In fact, about 90 percent of deceased victims of hypothermia
have detectable blood alcohol levels.
Urine Toxicology
As mentioned above, drug intoxication is both a causative and contributing
factor to hypothermia. Patients who present with altered mental status should
undergo urine toxicologic screening. This is especially useful in detecting or
ruling out suspected specific drugs. The clinician needs to remember that
urine toxicology reports may appear positive even after the intoxication has
been resolved.
Diagnostic Imaging Studies
Diagnostic imaging studies that may help pinpoint underlying contributing
factors to hypothermia or help guide management decisions include x-rays,
ultrasound, CT scan, and electrocardiogram.
X-ray
Chest x-ray (CXR) should be considered for hypothermic patients with altered
mental status since they are particularly at greater risk for aspiration
pneumonia.
Ultrasound
Currently, ultrasound is not specifically indicated in hypothermic patients.
However, an emergency department bedside ultrasound has a recognized role
in assessment for contributing factors of altered mental status: A Focused
Assessment with Sonography in Trauma (FAST) examination assesses for free
fluid, which is indicative of trauma or eroding intra-abdominal processes. In
addition, ultrasound can also be used to assess for pericardial effusion,
contractility, and dysfunctional wall motion.
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CT Scan
Like ultrasound, a CT scan is not clearly indicated for hypothermic patients,
although it can be particularly considered in those who continue to experience
altered mental status after re-warming to above 32°C. Once patients with
severe hypothermia has been stabilized, directed CT imaging, based on
patient signs and symptoms, may be initiated to find any underlying infection
or trauma.
Electrocardiography (ECG)
As mentioned previously, a hypothermic patient will have a reduced
spontaneous depolarization of pacemaker cells, prolonged action potential,
and
slowed
electroconduction
of
impulses
in
the
myocardium.
These
abnormalities are evident in ECG results, such as those listed below:

Prolonged intervals (PR, QRS, and QT)

Premature beats

Atrioventricular (AV) blocks

ST depressions and elevations

Bradycardia, and

Atrial and ventricular arrhythmias
Also, as mentioned previously, the characteristic ECG finding called the
Osborn wave or J-wave occurs in about 80 percent of hypothermic
patients.
The J-wave is a positive deflection at the QRS-ST junction. There is no clear
evidence on what specifically triggers the electrocardiographic formation of
the J-wave (Osborn wave). One hypothesis suggests that hypothermiainduced ion changes cause delayed depolarization or early repolarization of
the left ventricle. Another hypothesis suggests an unidentified hypothalamic
or neurogenic factor. The characteristic J-wave is seen in the majority of
hypothermic patients, regardless of the degree of hypothermia. Some studies
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have found proof that the absolute size of the J-wave is associated to the
temperature as hypothermia slowly resolves during the period of time that the
patient is rewarmed.
Other Studies
Patients who have no clear source of cold exposure and remain unresponsive
to rewarming efforts should be considered for testing for underlying etiologies
such as hypothyroidism and adrenal insufficiency.
Common Situations Resulting in Hypothermia
Trauma
Shock and cerebrospinal injury can destabilize thermoregulation. This is why
patients with multiple traumas or with CNS trauma are prone to hypothermia.
As mentioned previously, hypothermia exacerbates bleeding and increases
transfusion demands. It may also increase mortality. Coagulation factor
activity and platelet function decrease in response to declining temperatures,
leading to critical coagulopathy below 34°C. A combination of coagulopathy,
acidosis and hypothermia is often known as the death triad.
Burial Avalanche
About 150 people die due to being buried in avalanches each year in North
America and Europe. Fatalities are alleged to be greater in developing
countries. There are four major factors that affect survival of victims of
avalanche burial:
1. Grade of burial
2. Duration of burial
3. Presence of an air pocket or patent airway
4. Degree of trauma
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Based on the Swiss report, the overall mortality rate with avalanche burial is
23%, although this number primarily is dictated by the grade of burial. The
mortality rate for victims who are completely buried in snow is 52.4%, while
those who are partially buried only have a 4.2% rate.
Avalanche victims pulled from underneath deep snow has greater likelihood of
survival if burial time is no more than 35 minutes because the risk of
developing severe hypothermia is unlikely. This is because there is inadequate
cooling time. Individuals buried in snow can lose heat (cool down) at a
maximum rate of 9°C per hour. If such patients present with absent vital
signs, trauma and hypoxia should be highly suspected. If the burial time is
more than 35 minutes, the airway is obstructed with snow, and the patient is
asystolic, there is good chance that hypoxia occurred prior to hypothermia. On
the other hand, if the burial time exceeded 35 minutes and the airway
remained unobstructed, severe hypothermia should be highly suspected and
the patient should be treated accordingly.
In cases where the burial time is unknown, the core temperature can be used
to estimate it. A core temperature below 32°C is associated with a burial time
exceeding 35 minutes.
Cold Water Submersion
Cold-water submersion offers better outcomes than warm water submersion.
If the patient’s body was exposed to cold water with breathing intact, there is
great likelihood that the core temperature declined prior to the onset of
hypoxia and cardiac arrest (stage HT IV).
Survival is also possible without neurologic impairment. Conversely, if the
patient’s body was exposed to cold water and the breathing compromised
prior to cooling, the prognosis may be worse. The maximum-recorded time of
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cold water submersion correlated with survival without neurologic impairment
was 66 minutes in a child who was two and a half years old.
Frostbites
The American College of Surgeons (ACS) classifies frostbite based on the
severity of tissue injury. It is important to note that this classification cannot
be made until after re-warming efforts have been initiated, and in certain
cases, it may take up to 14 days for the severity of damage to be completely
revealed.
Regardless of the severity of the tissue injury, the majority of patients with
frostbite exhibit comparable initial symptoms. The area of the affected tissue
feels cold and numb, and prone to poor motor coordination. Rewarming the
affected area can lead to agonizing throbbing pain that may persist for several
weeks. Another symptom is electric shock sensations running through the
area of tissue injury. The frostbitten area may also develop sensory loss and
greater sensitivity to cold, which may persist for years. It is not uncommon
for arthritis and chronic neuropathic pain to develop in the affected area.
First-degree Frostbite
First-degree frostbite is shallow, involving the epidermis of the skin. It does
not affect the deeper tissues. Also known as frostnip, it is characterized by
skin accompanied numbness, swelling, and stiffness. The underlying tissue is
warm and soft. The skin may also appear mottled, red, white or yellowish.
Second-degree Frostbite
Second-degree frostbite is also superficial. It is characterized by white or
bluish skin that feels hard and frozen to touch.
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Clear or milky blisters usually develop within 24 hours of exposure to cold
stressors. These blisters are often surrounded by reddened and swollen skin.
The tissues beneath the injury remain.
Third degree Frostbite
Third degree frostbite involves the underlying tissues of the epidermis. Bloodfilled blisters that turn to black thick scabs and shed off spontaneously about
two weeks after the injury characterize this injury. The skin appears white,
blotchy or blue. The injured area feels hard and cold to touch.
Fourth degree Frostbite
Fourth degree frostbite is the most serious kind of frostbite. It affects the
underlying muscles, tendons, and bones, leading to tissue necrosis, gangrene,
and eventual loss of tissue. It causes severe pain deep in the joints. The skin
appears red or bluish which transforms into black. Upon inspection, the
affected area will not present with swelling, rather the skin over it feels
rubbery.
Treatment
Field Treatment
Field (pre-hospital) management measures for hypothermia are focused on
the following treatment priorities:

Inhibiting further heat loss

Re-warming the core temperature

Preventing the onset of fatal complications such as ventricular fibrillation
(VF) or other forms of arrhythmias
The cardiovascular consequences of hypothermia should be the top priority to
address. Mentally alert hypothermic patients can develop ventricular
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fibrillation suddenly with jerky and sudden movements. This is why prehospital rescue workers, especially those involved in remote search-andrescue operations should take care not to unnecessarily move these patients,
or if they must, must do so gently and carefully.
Patients who develop arrhythmias due to hypothermia in the field may
become unresponsive to resuscitation efforts. This is especially true among
those who were rescued from cold-water submersion. Rescuers are correct in
instructing such patients to reduce movements while waiting for careful
extrication.
The widely circulated anecdotal reports of sudden cardiac death linked with
tracheal intubation do not warrant attention, especially in cases of adequately
pre-oxygenated patients. The anticholinergic drug, atropine, and cardiac
pacing are not useful in managing bradyarrhythmias in hypothermic patients.
Likewise, lidocaine is also not useful in preventing hypothermia-induced
ventricular arrhythmias.
Anecdotal reports and several animal studies have found bretylium to be
effective in preventing sudden ventricular fibrillation in severely hypothermic
patients. In fact, some clinicians use the drug for that very same reason
under the following conditions:

Ventricular fibrillation developed at a core temperature of 30°C.

When the core temperature of the patient reached below 22°C since this
is the temperature which ventricular fibrillation is most likely to develop.

An initial dose of 5 mg/kg bretylium is recommended for all hypothermic
patients exhibiting apparent novel ventricular arrhythmias. The drug is
currently unavailable in the U.S. market.
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Rewarming efforts should be initiated in the field prior to hospital arrival by
rescuers and emergency responders to prevent the development of cardiac
arrhythmias with continued hypothermia. However, an exception to this
recommendation is in cases of frostbite injuries wherein rewarming efforts
directed towards the affected would rule it out because of pain.
The following are general rapid pre-hospital management and treatment
guidelines of hypothermic patients.

Gentle placement of patients in safe environments that prevent and/or
reduce further heat loss through evaporation, radiation, conduction, or
convection.

Removal of wet clothing, and securely placing patients within dry
blankets or sleeping bags.

Initiation of active external rewarming with heat packs such as chemical
packs and hot water bottles appropriately placed in the axillae, and on
the groin and abdomen.

Careful administration of rewarming techniques, with special caution
towards causing body surface burns from energetic active external
rewarming efforts.

In situations where heat packs are unavailable, rescuers and emergency
responders can provide skin-to-skin contact with patients to facilitate
rewarming using body heat.
Ventricular fibrillation presents a poor prognosis for hypothermic patients.
Generally, defibrillation is not effective when hypothermia has already set in
and when resuscitation equipment is unavailable. In cases like these, rescuers
or emergency responders should try a round of chemical conversion using
bretylium administered intravenously (if available), followed by extended
cardiopulmonary resuscitation (CPR) until such time that active re-warming
can be initiated and defibrillation performed successfully.
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Observing Vital Signs
Hypothermic patients need to be checked for vital signs including:

Temperature

Heart rate

Blood pressure

Respirations
Temperature
The majority of conventional clinical thermometers do not measure
temperatures less than 34°C. Esophageal thermometers can measure very
low core temperatures and may be employed to accurately assess the patient.
Another option is the use of a pulmonary catheter, which is partially invasive,
but very accurate since it is closest to the core. Its efficacy is superior
compared to rectal or bladder thermometers.
Heart Rate
Heart rate is usually fast in uncomplicated accidental hypothermia. It usually
persists until such time that the core temperature goes down below 29°C
(84.2°F) at which point, it slows down.
Blood Pressure
Blood pressure elevates in response to progressive hypothermia, at
temperatures as low as 27°C.89 This is a result of sympathetic stimulation by
the catecholamines released, which in turn cause greater vasoconstriction and
cardiac output. Patients with severe hypothermia often exhibit low blood
pressure due to volume alterations, cold diuresis, and dehydration.91
However, this is true for all patients, since hypothermic patients without
complications can maintain normal blood pressure even at temperatures as
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low as 25°C.90 It is critical to constantly monitor blood pressure levels to
prevent cardiovascular collapse during rewarming.
Respirations
Rapid breathing is usually present in mild and early hypothermia during the
sympathetic stimulation that occurs. This is often accompanied by severe
shivering. Conversely, the respiratory drive decreases, leading to slower
respiratory rate and shallow breathing once temperatures drop to less than
33°C. Other respiratory consequences are bronchorrhea and non-cardiogenic
pulmonary edema.
Oxygen Perfusion
Oxygen perfusion may be measured accurately using pulse oximetry, although
this may be difficult in patients with severe hypothermia due to the
consequent vasoconstriction. In these cases, measuring the arterial blood
gases (ABGs) may be the only way to evaluate oxygen perfusion.
Summary
This Part I Hypothermia course has discussed how individuals exposed to
freezing conditions become mild to profoundly hypothermic. Nurses and
rescue teams need to be educated and to be able to educate the public to the
signs and symptoms of the degrees of hypothermia that can occur, and the
prognosis based on the time exposed to or submerged in freezing conditions.
Thermoregulation involves transmission of cold sensation to hypothalamic
neurons through the thalamus and various nervous system tracks. Alterations
in the core temperature and impulses from nerves originating in the skin
directly affect temperature sensitive hypothalmic neurons. Both physiological
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biochemical factors and behavioral responses affect body temperature and
responses to adverse internal and external conditions.
While it’s important to understand the setting and history of the patient and
the condition when they are rescued, it’s also just as critical to intervene with
the right decision-making and rescue methods. Hypothermia Part II covers
more specific modified and advanced rescue measures.
Definition of Terms
Adrenal insufficiency: An endocrine disorder wherein the adrenal glands do
not produce adequate amounts of steroid hormones such as cortisol and
aldosterone.
Anoxic: An abnormal condition characterized by low amount of oxygen in the
body tissues.
Arteriovenous anastomoses: A blood vessel that connects an arteriole
directly to a venule.
Asystole: A cardiac standstill with no cardiac output and no ventricular
depolarization.
Bradycardia: A slow heart rate of less than 60 beats per minute.
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Chilblains: These are small, itchy, painful lumps that develop on the skin due
to capillary injuries. They develop as an abnormal response to cold.
Circadian rhythm: The body’s natural clock which dictates the patterns of
physiological and behavioral processes over a 24-hour period.
Core temperature after-drop: Refers to the phenomenon of continuous
core temperature decline despite re-warming efforts.
Debridement: Refers to the surgical removal of unhealthy tissue from a
wound to promote healing.
Eschar: Refers to dead tissue that sheds off from healthy skin following
injuries such frostbites, burns and pressure wounds.
Frostbite: A medical condition wherein peripheral tissues (i.e., foot, fingers,
toes) sustain localized damage due to severe cold.
Frostnip: An initial stage of frostbite characterized by a reddish and very cold
skin due to its frozen surface.
Gangrene: Refers to a type of tissue death which occurs due to loss of blood
supply.
Hyperkalemia: Refers to condition wherein the potassium level in the blood
which higher than normal.
Hypocapnia: It refers to a condition wherein the level of carbon dioxide in
the blood is lower than normal which can result from acapnia.
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Hypokalemia: Refers to a condition wherein there is lower than normal level
of potassium in the bloodstream.
Hypothermia: A medical emergency that happens when the body loses heat
faster than it can produce it, causing a dangerously low core temperature.
Hypopituitarism: An endocrine syndrome characterized by inadequate
pituitary hormone production. It usually is a result of disorders involving the
pituitary gland, hypothalamus, or surrounding structures.
Ischemia: Refers to a condition wherein the blood flow (and thus oxygen) is
restricted or reduced in a part of the body.
Normothermia: A condition of normal body temperature.
Paradoxical undressing: It refers to the phenomenon of removing all
articles of clothing shortly before death due to severe hypothermia.
Poikilothermic: An organism having a body temperature that fluctuates with
the temperature of its surroundings.
Set point: The temperature level at which there is a balance between heat
loss and heat production.
Terminal burrowing: It refers to the phenomenon of crawling into small
confined spaces after removing all articles of clothing (paradoxical undressing)
shortly before death due to severe hypothermia.
Thermoregulation: Also known as temperature homeostasis. It refers to the
process that allows the human body to maintain its core internal temperature.
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Thoracotomy: Refers to a surgical incision into the pleural space of the chest
to access the lungs, heart and other adjacent organs or insertion of
mechanical ventilation.
Trench foot: Also known as immersion foot. It refers to an injury of the skin,
blood vessels, and nerves of the feet due to prolonged exposure to cold and
wet terrains.
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1. The normal adult temperature ranges from 36-38°C, depending
on many internal factors such as:
a.
b.
c.
d.
Wind movement
Circadian rhythm
Humidity
Nature of surrounding environment
2. Which of the following neuronal effector mechanisms activated
by cold stimuli increase heat production?
a.
b.
c.
d.
Shivering
Cutaneous vasodilation
Piloerection Humidity
Sweating
3. Which clinical findings can be seen in patients with mild
hypothermia?
a.
b.
c.
d.
Diminished shivering
Slow stretch reflexes
Stiff muscles and joints
Cold-induced diuresis
4. Which mechanism of environmental heat loss is exemplified by
the dissipation of up to 50 percent of the body’s heat through an
uncovered head?
a.
b.
c.
d.
Convection
Conduction
Radiation
Evaporation
5. Which mechanism of environmental heat loss is exemplified by
excessive sweating?
a.
b.
c.
d.
Convection
Conduction
Radiation
Evaporation
6. True or False: The presence of the characteristic J-wave or
Osborne wave on the ECG is diagnostic for hypothermia.
a. True
b. False
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7. Which of the following disorders is caused by impaired
hypothalamic thermoregulation and predispose individuals to
hypothermia?
a.
b.
c.
d.
Acute renal failure
Wernicke’s encephalopathy
Hypothyroidism
Hypoglycemia
8. Which of the following complications of hypothermia is
characterized by the victim’s removal of clothes just before
death?
a.
b.
c.
d.
Voluntary behavior modification
Involuntary behavior modification
Terminal burrowing
Paradoxical undressing
9. Which of the following cold injuries refers to an injury of the
foot/feet due to prolonged exposure to wet and cold terrains?
a.
b.
c.
d.
Second degree frostbite
Frostnip
Trench foot
Chilblains
10. The cold-induced diuresis, which occurs during mild
hypothermia, is due to which of the following physiological
mechanisms?
a.
b.
c.
d.
Enhanced renal blood flow following vasoconstriction
Inhibition of ADH
Enhanced urinary electrolyte excretion
Increased distal tubular reabsorption of water
11. _________________ is a pathologic condition wherein the
core body temperature is less than 35°C.
a.
b.
c.
d.
Thermogenesis
Failed thermoregulation
Hyperthermia
Hypothermia
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12. True or False: The core body temperature, such as esophageal
and rectal, is normally 0.5°C greater than the oral temperature.
a. True
b. False
13. Due to the circadian rhythm, body temperature fluctuates more
or less 0.6°C
a.
b.
c.
d.
between meals.
between the morning and evening.
during exercising.
between body organs and the skin surface.
14. Women experience core body temperature changes during
their monthly menstrual cycle: It _____________________
during ovulation and returns to normal when menstruation
begins.
a.
b.
c.
d.
increases by 0.5°C
decreases by 0.6°C
rises as high as 40°C
falls to less than 35°C
15. The posterior pituitary region is concerned with heat
maintenance. It contains a large number of ____________
nerve cells.
a.
b.
c.
d.
hot- and cold-sensitive
heat-sensitive
cold-sensitive
poikilothermic-sensitive
16. True or False: The skin contains both cold and warmth
receptors. The number of cold receptors is ten times more than
the warmth or heat receptors.
a. True
b. False
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17. Piloerection, which produces “goose bumps,” is caused by
sympathetic stimulation of the _____________________
attached to the hair follicles.
a.
b.
c.
d.
neurotransmitters
sympathetic nerves
arrector pili muscles
brown fat cells
18. The increase in cellular metabolic activity, caused by the
thyroid-stimulating hormone (TSH),
a.
b.
c.
d.
results instantaneously in thyroid gland hypertrophy.
causes “goose bumps.”
happen instantaneously.
does not happen instantaneously.
19. Toxic thyroid goiters is found more frequently in individuals
who
a.
b.
c.
d.
change climates often.
reside long periods in cold climates.
live long periods in hot climates.
often have a body core temperature above 37.1°C.
20. The temperature set point in the hypothalamus is determined
mainly by the intensity of activity of the heat thermoreceptors
a.
b.
c.
d.
in the anterior hypothalamus.
in the skin.
in the spinal cord tissues.
hypothalamic thermoregulation center.
21. When the skin temperature is high, ____________ begins at a
lower hypothalamic temperature compared to when the skin
temperature is low.
a.
b.
c.
d.
shivering
sweating
excessive heat loss
activity
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22. True or False: When the skin encounters cold stimuli, the
hypothalamic centers are activated towards the shivering
threshold even when the hypothalamic temperature may be
normal.
a. True
b. False
23. When an individual puts a foot under a hot lamp and leaves it
there for a few minutes, local capillaries __________ and mild
local sweating occurs.
a.
b.
c.
d.
slow
constrict
dilate
reflex
24. Sweating starts and stops due to temperature changes directly
on the blood vessels and also by local cord reflexes that run
first from skin receptors to
a.
b.
c.
d.
the
the
the
the
hypothalamic center.
sweat glands.
brain.
spinal cord.
25. When the internal body temperature increases significantly,
signals from the _________________________ sends out a
psychic sensation of overheat.
a.
b.
c.
d.
skin
visceral tissue receptors
anterior and posterior hypothalamus
anterior hypothalamus
26. The only effective mechanism that retains body heat in
extremely cold environments is
a.
b.
c.
d.
local capillary dilation.
the activity of the individual’s heat thermoreceptors.
the body’s involuntary mechanism of thermoregulation.
the individual taking action to warm his or her body.
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27. Traditionally, hypothermia has been classified into three
categories. A person classified as moderate hypothermia has a
body core temperature between
a.
b.
c.
d.
28-32°C.
32-35°C.
35-40°C.
25-29°C.
28. True or False: Skin disorders and injuries such as psoriasis and
burns decrease the body's ability to preserve heat.
a. True
b. False
29. If glycogen stores in the liver are exhausted, hypoglycemia
may occur which inhibits
a.
b.
c.
d.
sweating.
shivering.
vasoconstriction.
capillary dilation.
30. Active re-warming must be initiated when the core
temperature falls below _____ because below that
temperature, an individual cannot spontaneously return to the
set point (the normal core body temperature of about 37°C).
a.
b.
c.
d.
28°C.
30°C.
34°C.
25°C.
31. ___________________ accounts for about 15 percent of heat
loss.
a.
b.
c.
d.
Conduction
Radiation
Sweating
Thermogenesis
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32. Evaporation accounts for approximately ___ percent of heat
loss.
a.
b.
c.
d.
50
15
20
40
33. Hypothermia also causes cellular membrane disruption,
allowing intracellular fluid to leak out, and ultimately leading
to electrolyte imbalance, particularly
a.
b.
c.
d.
hypertrophy.
poikilothermia.
hyperglycemia.
hyperkalemia.
34. True or False: Cold infusions, rapid treatment of heatstroke,
and emergency deliveries do NOT cause hypothermia.
a. True
b. False
35. Endocrine dysfunctions, such as __________________, are
known causes of decreased heat production.
a.
b.
c.
d.
severe anorexia
poikilothermia
Parkinson’s disease
adrenal insufficiency
36. In patients presenting with unexplained hypothermia who fail
to re-warm with conventional treatment modalities, causes
may include
a.
b.
c.
d.
severe anorexia
hypoglycemia
Parkinson’s disease
All of the above
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37. Therapeutic doses of ______________ have been reported to
cause a drop in core temperature.
a.
b.
c.
d.
valproic acid
lithium
antidepressents
All of the above
38. True or False: Phenothiazines can cause central
thermoregulation dysfunction and inhibition of peripheral
vasoconstriction in response to cold through their blockade of
alpha-receptors.
a. True
b. False
39. Among the elderly, the most common precipitating factor for
hypothermia is
a.
b.
c.
d.
presence of brown adipose tissue in the elderly.
increased lean body mass.
sepsis (systemic infection).
hypothyroidism.
40. Trench foot occurs in part because wet feet lose heat
_________ faster than dry feet.
a.
b.
c.
d.
25-times
twice
10%
three-times
41. True or False: Numerous studies from the Scandinavian
countries found hypothermia may be delayed by the victim
smoking.
a. True
b. False
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42. ______________ is caused by the movement of extracellular
potassium into the cells, stimulated by alterations in cell
membrane permeability and the activity of the sodiumpotassium pump.
a.
b.
c.
d.
Hypertrophy
Poikilothermia
Hypokalemia
Hypothyroidism
43. Ischemia, amplified adrenergic activity and electrolyte
imbalance help lead to myocardial instability such as
arrhythmias in cases of ____________ hypothermia.
a.
b.
c.
d.
moderate
severe
mild
All of the above
44. Hypothermia can also interfere with endothelial synthesis of
prostacyclin (PGI2) and its inhibitory action on platelet
aggregation, triggering platelet activation and
a.
b.
c.
d.
anemia.
hypokalemia.
thrombosis.
alkalosis.
45. Hypothermia, postmortem patients who showed evidence of a
mild increase in serum amylase, which means that the
___________ is/are also affected by hypothermia.
a.
b.
c.
d.
kidneys
capillaries
liver
pancreas
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Correct Answers:
1. The normal adult temperature ranges from 36-38°C, depending
on many internal factors such as:
b. Circadian rhythm
2. Which of the following neuronal effector mechanisms activated
by cold stimuli increase heat production?
a. Shivering
3. Which clinical findings can be seen in patients with mild
hypothermia?
d. Cold-induced diuresis
4. Which mechanism of environmental heat loss is exemplified by
the dissipation of up to 50 percent of the body’s heat through an
uncovered head?
c. Radiation
5. Which mechanism of environmental heat loss is exemplified by
excessive sweating?
d. Evaporation
6. True or False: The presence of the characteristic J-wave or
Osborne wave on the ECG is diagnostic for hypothermia.
b. False
7. Which of the following disorders is caused by impaired
hypothalamic thermoregulation and predispose individuals to
hypothermia?
b. Wernicke’s encephalopathy
8. Which of the following complications of hypothermia is
characterized by the victim’s removal of clothes just before
death?
d. Paradoxical undressing
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9. Which of the following cold injuries refers to an injury of the
foot/feet due to prolonged exposure to wet and cold terrains?
c. Trench foot
10. The cold-induced diuresis, which occurs during mild
hypothermia, is due to which of the following physiological
mechanisms?
a. Enhanced renal blood flow following vasoconstriction
11. _________________ is a pathologic condition wherein the
core body temperature is less than 35°C.
d. Hypothermia
12. True or False: The core body temperature, such as esophageal
and rectal, is normally 0.5°C greater than the oral temperature.
a. True
13. Due to the circadian rhythm, body temperature fluctuates more
or less 0.6°C
b. between the morning and evening.
14. Women experience core body temperature changes during
their monthly menstrual cycle: It _____________________
during ovulation and returns to normal when menstruation
begins.
a. increases by 0.5°C
15. The posterior pituitary region is concerned with heat
maintenance. It contains a large number of ____________
nerve cells.
c. cold-sensitive
16. True or False: The skin contains both cold and warmth
receptors. The number of cold receptors is ten times more than
the warmth or heat receptors.
a. True
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17. Piloerection, which produces “goose bumps,” is caused by
sympathetic stimulation of the _____________________
attached to the hair follicles.
c. arrector pili muscles
18. The increase in cellular metabolic activity, caused by the
thyroid-stimulating hormone (TSH),
d. does not happen instantaneously.
19. Toxic thyroid goiters is found more frequently in individuals
who
b. reside long periods in cold climates.
20. The temperature set point in the hypothalamus is determined
mainly by which of the following intensity of activity of the
heat thermoreceptors
a. in the anterior hypothalamus.
21. When the skin temperature is high, ____________ begins at a
lower hypothalamic temperature compared to when the skin
temperature is low.
b. sweating
22. True or False: When the skin encounters cold stimuli, the
hypothalamic centers are activated towards the shivering
threshold even when the hypothalamic temperature may be
normal.
a. True
23. When an individual puts a foot under a hot lamp and leaves it
there for a few minutes, local capillaries __________ and mild
local sweating occurs.
c. dilate
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24. Sweating starts and stops due to temperature changes directly
on the blood vessels and also by local cord reflexes that run
first from skin receptors to
d. the spinal cord.
25. When the internal body temperature increases significantly,
signals from the _________________________ sends out a
psychic sensation of overheat.
c. anterior and posterior hypothalamus
26. The only effective mechanism that retains body heat in
extremely cold environments is
d. the individual taking action to warm his or her body.
27. Traditionally, hypothermia has been classified into three
categories. A person classified as moderate hypothermia has a
body core temperature between
a. 28-32°C.
28. True or False: Skin disorders and injuries such as psoriasis and
burns decrease the body's ability to preserve heat.
a. True
29. If glycogen stores in the liver are exhausted, hypoglycemia
may occur which inhibits
b. shivering.
30. Active re-warming must be initiated when the core
temperature falls below _____ because below that
temperature, an individual cannot spontaneously return to the
set point (the normal core body temperature of about 37°C).
b. 30°C.
31. ___________________ accounts for about 15 percent of heat
loss.
a. Conduction
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32. Evaporation accounts for approximately ___ percent of heat
loss.
c. 20
33. Hypothermia also causes cellular membrane disruption,
allowing intracellular fluid to leak out, and ultimately leading
to electrolyte imbalance, particularly
d. hyperkalemia.
34. True or False: Cold infusions, rapid treatment of heatstroke,
and emergency deliveries do NOT cause hypothermia.
b. False
35. Endocrine dysfunctions, such as __________________, are
known causes of decreased heat production.
d. adrenal insufficiency
36. In patients presenting with unexplained hypothermia who fail
to re-warm with conventional treatment modalities, causes
may include
d. All of the above
37. Therapeutic doses of ______________ have been reported to
cause a drop in core temperature.
a. valproic acid
38. True or False: Phenothiazines can cause central
thermoregulation dysfunction and inhibition of peripheral
vasoconstriction in response to cold through their blockade of
alpha-receptors.
a. True
39. Among the elderly, the most common precipitating factor for
hypothermia is
c. sepsis (systemic infection).
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40. Trench foot occurs in part because wet feet lose heat
_________ faster than dry feet.
a. 25-times
41. True or False: Numerous studies from the Scandinavian
countries found hypothermia may be delayed by the victim
smoking.
b. False
42. ______________ is caused by the movement of extracellular
potassium into the cells, stimulated by alterations in cell
membrane permeability and the activity of the sodiumpotassium pump.
c. Hypokalemia
43. Ischemia, amplified adrenergic activity and electrolyte
imbalance help lead to myocardial instability such as
arrhythmias in cases of ____________ hypothermia.
a. moderate
44. Hypothermia can also interfere with endothelial synthesis of
prostacyclin (PGI2) and its inhibitory action on platelet
aggregation, triggering platelet activation and
c. thrombosis.
45. Hypothermia, postmortem patients who showed evidence of a
mild increase in serum amylase, which means that the
___________ is/are also affected by hypothermia.
d. pancreas
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References Section
The reference section of in-text citations include published works intended as
helpful material for further reading. Unpublished works and personal
communications are not included in this section, although may appear within
the study text.
1. Centers of Disease Control and Prevention (2015). Hypothermia-Related
Deaths — Wisconsin, 2014, and United States, 2003–2013.
64(06);141-143. Retrieved online at
https://www.cdc.gov/mmwr/preview/mmwrhtml/mm6406a2.htm.
2. Noe, Rebecca S., et al. (2012). Exposure to Natural Cold and Heat:
Hypothermia and Hyperthermia Medicare Claims, United States, 2004–2005.
American Journal of Public Health: April 2012; Vol 102, No. 4.
3. Hall, J. (2011). Regulation of body temperature: role of the hypothalamus.
Guyton and Hall Textbook of Medical Physiology.
4. Brown, D.J.A., Brugger, H., Boyd, J. & Paal, P. (2012). Accidental
hypothermia. New England Journal of Medicine, 367;20. Retrieved from
http://www.uphs.upenn.edu/ppmc_emergency/PPMC%20Bookmarks/2015%2
0LLSA%20Articles/Accidental%20Hypothermia.pdf.
5. O’Connell, J., Petrella, D., & Regan, R. (Accidental hypothermia and
frostbite: cold-related conditions. The Healthcare for Homeless Persons.
Retrieved from
http://www.bhchp.org/BHCHP%20Manual/pdf_files/Part2_PDF/Hypothermia.p
df.
6. Lallanilla, M. (2013). Get naked and dig: The bizarre effects of
hypothermia. Retrieved from http://www.livescience.com/41730hypothermia-terminal-burrowing-paradoxical-undressing.html
7. Danzl, D.F. Accidental hypothermia. In: Auerbach PS, ed. Wilderness
medicine. 6th ed. Philadelphia: Mosby, 2012:116-42
8. Putzer, G., Schmid, S., Braun, P., Brugger, H., & Paal, P. (2010). Cooling of
six centigrades in an hour during avalanche burial. Resuscitation, 81:1043-4
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73
9. Vanden-Hoek, T.L., Morrison, L.J., & Shuster, M. (2010). Part 12: cardiac
arrest in special situations: 2010 American Heart Association Guidelines for
Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
Circulation, 122:Suppl 3:S829-S861. [Errata, Circulation 2011;123(6):e239,
2011;124(15):e405.]
10. Soar, J., Perkins, G.D., Abbas, G. (2010). European Resuscitation Council
Guidelines for Resuscitation 2010 Section 8: cardiac arrest in special
circumstances: electrolyte abnormalities, poisoning, drowning, accidental
hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma,
pregnancy, electrocution. Resuscitation, 81:1400-33.
11. Brugger, H., Paal, P., & Boyd, J. (2011). Prehospital resuscitation of the
buried avalanche victim. High Altitude Medicine and Biology, 12:199-205.
12. Boyd, J., Brugger, H., & Shuster, M. (2010). Prognostic factors in
avalanche resuscitation: a systematic review. Resuscitation, 81:645-52.
13. Tipton, M.J, & Golden, F.S. (2011). A proposed decision-making guide for
the search, rescue and resuscitation of submersion (head under) victims
based on expert opinion. Resuscitation, 82:819-24.
14. Perlman, R., et al. (2016). A recommended early goal-directed
management guideline for the prevention of hypothermia-related transfusion,
morbidity, and mortality in severely injured trauma patients. Critical Care
(2016) 20:107 DOI 10.1186/s13054-016-1271-z.
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