29

H YPOTHERMIA IN T R AU M A

Eldar Sreide and Charles E. Smith

Objectives
Provide a thorough understanding of the clinical impact of hypothermia in trauma patients.

Provide a clinically useful guide to the differentiation between mild, moderate, and severe
trauma-associated hypothermia.
Present the current knowledge on prevention and treatment of hypothermia in trauma victims,
with a special focus on critical bleeding.
Understand the mechanisms and the diagnosis and treatment of accidental hypothermia with
and without asphyxia.
understanding of hypothermia associated with
trauma, with the main focus being on clinical
management.

INTRODUCTION

The anesthesiologist can play many important

roles in the Trauma Chain of Survival (Figure
29.1). In some systems, the contribution of the
anesthesiologist is limited to perioperative care,
while in other systems the anesthesiologist acts
both as a prehospital emergency physician, as a
member of the hospital trauma team, and as a
critical care physician. Independent of where and
what role, hypothermia is a serious complication
to trauma that deserves full attention by the
anesthesiologist [13]. As hypothermia is
generally considered detrimental for the patient,
much focus has been on prevention. Despite this,
hypothermia in trauma patients is still a common
finding. There are many indications that
hypothermia is still not managed in an optimal
fashion [3, 4].

Based on promising animal results, some

authors believe that rapidly induced extreme
hypothermia (hibernation) may play a future
role in severe hemorrhagic shock during transport
to definitive surgical care [5]. So far, this
laboratory research has not changed clinical
practice and probably will not do so in the near
future. On the other hand, in patients with trau-
matic brain injury, induction of mild hypothermia
(therapeu-tic hypothermia) has become a
promising treatment modal-ity [6]. Hypothermia
may also develop without concurrent trauma
(accidental hypothermia) [7]. The aim of this
chap-ter is to present an overview of our current

T H E R M O R E G U L AT I O N A N D T H
E R M AL
M A N AG E M E N T
Thermoregulation in Humans
In humans, the core temperature remains stable
within a nar-row temperature range despite large
variations in environmen-tal conditions [8, 9]. To
achieve this we have several mecha-nisms
helping us. In the thermoneutral zone (TNZ) the
basal metabolic rate is producing enough heat to
prevent a fall in core temperature, while not
increasing it [8, 9]. The insula-tion (clothing and
other protective layers) is the most impor-tant
445
factor defining the TNZ in humans (Figures
29.229.4). Outside the TNZ, two main
involuntary mechanisms will act to maintain a
stable core temperature: shivering to produce
heat and sweating to eliminate heat (Figures
29.229.4). From a metabolic point of view, both
these autonomic mechanisms are costly to the
body.
The most effective thermoregulatory
response is behavioral (Table 29.1). For example,
conscious humans respond to the surrounding
conditions appropriately to avoid a decrease or
increase in core temperature (e.g., clothing,
seeking shelter). Another effective and
metabolically inexpensive thermoregu-latory
response is the change in vasomotor tone in the
arteri-ovenous shunt to either minimize heat loss
through the skin or to increase it (Figure 29.3).
The dominating afferent thermal signal to the
brain comes from both nonthermospecific and
thermospecific (cold or warm) receptors located
in the skin and mucous membranes
446 S oR E I D E AN D S MITH

f
a
rly ir st ai
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t
o

p
r
e
v
e
n
t
i
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m
ed
i
a o
n
t ti
e ra
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se
 a
r
ly r
eh bi
lit a ti
a o
E
n
v.the ra
d
a p
ly y
r

a
E

li
f
o
t o li
t
y

re u
a

storeq
t y
o l r
i ju
mi irin
t

orrepa
much quicker
Figure 29.1.
than adults due
Trauma Chain
of Survival. to their large
Reproduced surface
with permission compared with
from Laerdal their metabolic
Medical Inc. rate. On the
other hand,
exter-nal
rewarming is
[10]. When much more
the afferent
thermal effective in
signals reach children.
the Chronic ill-
hypothalamus ness is one of
(the control
center), they the many
are integrated factors
with other predisposing
information individuals to
and then
result in an the
efferent development of
response hypothermia
(cold or (Table 29.2).
warm)
(Figures 29.2
and 29.3).
The exception Effect of
is when the Anesthesia
person is in and Surgery
the TNZ, also
called the (Perioperativ
set-point e
temperature Hypothermi
or the a)
interthreshol
d range [8 Factors
10]. This is predisposing
the narrow patients to

range (0.4 C) perioperative
around the
normal core hypothermia
temperature are the same as

of 37.0 C at those
which there is predisposing
no efferent conscious
response.
This set point individuals for
may fluctuate hypothermia
with time of (Table 29.2).
day, sex, and However,
acclimation.
Both the induction of
body general anes-
morphology thesia results in
and age will an immediate
influence the decrease in
ther- core
moregulatory temperature [9,
response and 14]. The first
capacity [11 temperature
13]. Infants and fall (first phase
chil-dren cool of
perioperative
hypothermia) is
due to Figure 29.3.
anesthetic Environmental
drug-induced temperature and
peripheral blood
vasodilatation
flow. Within the
causing heat
TNZ heat loss
distribution to
from the body is
the peripheral
manipulated by
compartment
adjusting
[15 21]. All
vasomotor tone.
general
Heat exchange
anesthetics
between the
with the
body core and
exception of
the envi-
ketamine affect
ronment is
the normal
determined by
thermoregulato
the amount of
ry responses in
blood flowing
the same
through the
manner,
subcutaneous
heat exchange
vascular
structures
located in the
periph-ery.
Arteriovenous
anastomoses
(AVAs) regulate
blood flow
through the
subcutaneous
layers. At the
lower limit of
the TNZ the
lower critical
temperature
(LCT) all of
the AVAs are
closed and
blood flow
through the heat
exchangers is
minimal. At the
upper limit of
the TNZ the
upper critical
temperature
(UCT) all of
the AVAs are
open and blood
flow through the
heat exchangers
is maximal.
Reproduced
from reference 8
with permission.

but to a
different
degree [9, 12,
14, 2228].
This results in
the
interthreshold by a slower
range decrease until
expanding up the plateau
phase when the
to 4 C (Figure
29.5). The net thermoregulato
effect is a rapid ry
fall in core compensatory
mechanisms
temperature (1 kick in

C1.5 C) (primarily
during the first vasoconstrictio
hour, followed n). The surgical
procedure

Figure 29.4.
Environmental
temperature and
metabolic rate.
Within the TNZ
metabolic rate is
Figure 29.2. The low and
insulation value constant; the
of clothing individual
determines the thermoregulates
environ-mental by adjusting
range of the vasomotor tone
thermoneutral to control heat
zone (TNZ). loss from the
The greater the thermal core.
insula-tion, the Above the UCT
lower the TNZ. the individual
Humans have must expend
the unique energy on heat
ability to alter loss (sweat-ing)
their to maintain the
supracutanous desired
insulation layer. temperature.
Reproduced Below the LCT
from reference 8 the individual
with per- must increase
mission. the metabolic
heat production
(shivering) to
compensate for
the increased
heat loss to the
environment. If
the capacity to
com-pensate for
the environment
fails, body core
temperature will
fall (or increase)
and eventually
death will
ensue.
Reproduced
from reference 8
with permission.
Table 29.1:
Thermoregulat
ion: Behavioral H YP
and OTHE
RMIA
Autonomic
IN T
Responses RAU M
A

System Examples
447
Behavioral Adjusting clothing
Modifying
Tableenvironmental
29.2: temperature (heating, air
conditioning)
Predisposing
Voluntary movements
Factors for and timing of activities.
Hypothermia
Autonomic Vasodilation. Promotes either heat loss or heat gain
depending
Mechanismon environmental conditions.
Examples
Vasoconstriction. Cutaneous blood flow decreases
to near zero in
Impaired cold temperatures.
thermoregu- Drugs: alcohol, general and regional
Heartlation
rate. Pulse is often higher foranesthesia,
and decreased any given tricyclic
core antidepressants,
temperature during heating than phenothiazines,
heat production during cooling, antipyretics.
thus increasing heat transfer viaImpaired
the bloodneurologic state and mobility:
Piloerection. Increases insulation; e.g.,
slowsbrain
heatinjury, stroke, spinal cord
exchange. injury, severe trauma, shock
Increased body fat. Fat conducts Extremes
heat only of age
one-third as fast as other tissues.Autonomic nervous system dysfunction
Shivering. Increases heat production when
Chronic the skin
illness with hypometabolic
and/or body is cold. features such as heart failure,
Nonshivering thermogenesis. Increases heat
hypothyroidism, adrenal disease,
production without muscular activity. The
diabetes, malnutrition
principal heat producers are theSevere
liver, kidney, and
sepsis (bacterial toxins)
brain via brown adipose tissue whose sole
Increased
function is to heat loss heat in neonates.
produce Neonates and infants: increased body
Evaporation. Increased amount of surfacesweatingarea to mass ratio
Cold environmental temperature
Exposure to windy and wet climate,
Modified from submersion/immersion
Kabbara A,
Poor socioeconomic status
Smith CE.
Monitoring Burns
temperature. Large blood loss
In Wilson WC, Exposed abdominal and/or thoracic
Grande CM, contents
Hoyt DB, ed. General and neuraxial anesthesia
Trauma: Geriatrics
Resuscitation,
Thin body habitus
Anesthesia,
and Critical
Low skin-surface temperature of
Care. New patient prior to injury
York: Taylor
& Francis
Modified from
Group, 2006.
Smith CE,
Reproduced
Patel N.
with Hypothermia
permission. in adult trauma
patients:
Anesthetic
considerations.
Part I. Etiology
and
pathophysiolog
y. Am J
Anesthesiol
1996;23:283
90.
 further
increases the
Figure 29.5. risk for
Activation of hypothermia
thermoregulatory if large body
effector surface areas
responses is trig- are exposed
gered at specific over a
temperatures for prolonged
a given time.
individual Moreover,
(threshold replacement
temper-ature). of shed blood
Under general with cold or
anesthesia, the inadequately
threshold for warmed IV
temperatures for fluids and
activation of cold blood can
effector significantly
responses decrease body
(including temperature
vasoconstriction [9, 12, 14].
and shivering) The larger the
are lowered, gradient
whereas those for between the
activation of temperature
warm responses of the infused
(including fluid and core
sweating and temperature,
vasodilation) are
the greater
increased. Thus,
the drop in
the interthreshold
mean body
range is widened
temperature.
As well, the
during general
greater the
anesthesia to

fluid
about 4 C. requirement
Reproduced with relative to
permission from body weight,
reference 10. the greater
the potential
drop in body
temper-ature.
Epidural
and spinal
anesthesia also
impair
peripheral and
central
thermoregulati
on [9, 14]. The
initial
vasodilation in
the conscious
patient may
cause the
patient to feel
warm, but a
dis-turbing
shivering may
follow as the
temperature
falls. Although
the
mechanisms
behind the
disturbed
thermoregulati
on are more rewarming
complicated [29].
with regional
than general
Side Effects
anesthesia, the
of
net effect is the
same; a
Perioperativ
dangerous fall e
in core Hypothermi
temperature [9, a
14]. The general
Vasodilation effect of
induced by cooling is that
regional all body
anesthesia may, processes,
however, includ-ing
accelerate the neuromuscular
temperature function [13,
increase during 30, 31], slow
down to the
448 S oR immunosuppression, including
E I D E AN DSM reduced T-cell-mediated
ITH
antibody production and reduced
nonspecific oxidative bacterial
Table 29.3: killing by neutrophils
Pathophysiolo Decreased collagen deposition
gic
Consequences
and Modified from
Complications Smith CE,
from
Perioperative Yamat RA.
and Trauma- Avoiding
Associated hypothermia in
Hypothermia the trauma
patient. Curr
System Affected Opin
Anaesthesiol
2000;13:167
Impaired cardiorespiratory
74. Reproduced
function with
permission.

stage of
depression
and
eventually
death (Figure
29.4). Even
moderate
degrees of
Impaired coagulation hypothermia
will produce
clinically sig-
nificant
Impaired hepatorenalnegative
function and decreasedeffects
drug in
most
clearance (anesthetics!) organ
systems [13,
30, 31]. They
have a
significant
Impaired resistance toimpact on
outcome in
infections (pneumonia,
periopera-tive
sepsis, wound infections)
and trauma-
Impaired wound healing.
associated
hypothermia
(Table 29.3)
[13, 9, 32
35]. Table 29.4:
Although Mechanisms of
the general Heat Loss
definition of
hypothermia is Mechanism Description
a core
temperature of Radiation Transmission of heat energy from exposed skin

less than 35 C to cooler surroundings via electromagnetic
[36], even waves according to the temperature difference
milder of the objects.
deviations from
the normal Conduction Transfer of heat energy between two solid
temperature objects in contact according to the thermal
may result in conductivity of the objects, area in contact, and
significant
thermal gradient (e.g., transfer of heat due to
morbidity and
mortality in direct contact of skin and viscera with colder
surgical objects such as bed, spine backboard, and
patients. For surrounding air; e.g., transfer of heat from
example, patients blood to unwarmed or inadequately
decreases in warmed IV fluids)
intra-operative
temperatures to Convection Transfer of heat energy during the mass

between 34 C movement of gas or liquid

and 36 C have Evaporation Heat energy transferred during change of phase
been associated (water to gas): 58 kcal/g water evaporated from
with a
significant skin, respiratory tract, and viscera.
increase in Redistribution Redistribution of warmer core blood to the
complications
such as cooler periphery due to anesthetic agents (e.g.,
shivering, propofol, inhalational agents, alcohol
postoperative intoxication). Subsequent heat loss by other
wound mechanisms.
infections,
perioperative
bleed-ing and Modified from
transfusion Smith CE, Patel
requirements, N. Hypothermia
cardiac events in adult trauma
(myocardial patients:
anesthetic
considerations.
Part I. Etiology
and
pathophysiolog
y. Am J
Anesthesiol
1996;23:283
90; Wilson WC,
Smith CE, Haan
J, Elamin EM.
Hypothermia
and heat-related
injuries. In
Wilson WC,
Grande CM,
Hoyt DB, ed.
Trauma:
Resuscitation,
Anesthesia, and
Critical Care.
New York:
Taylor &
Francis Group,
2006.
Reproduced
with
permission.
 perioperative
hypothermia or
ischemia, to rewarm
ventricular patients, it is
tachycardia), important to
as well as consider the
prolonged four alterna-
hospital stay
(Table 29.3) tives for heat
[9, 3235, transfer:
3740]. convection,
Important conduction,
ly, the effects radiation, and
of all evaporation
anesthetic (Table 29.4) [3,
drugs, 14]. All
including commercial
neuromuscula rewarming and
r blocking cooling
drugs, are
increased equipment
during available make
hypother-mia use of these
(Table 29.3) mecha-nisms.
[9, 35, 41]. Convection
There is a real represents heat
risk of transfer
overdosing through air that
the patient. is in contact
Neuromuscul with the body,
ar function
testing and its
becomes efficiency is
increasingly mostly
difficult at determined by
low air velocity.
temperatures Conductive
[41]. heat transfer
implies direct
contact
Rewarming between two
and objects and
Maintaining their
Normotherm characteristics.
ia Methods The rate of heat
and transfer from
Equipment an object to
Before fluid is 32
discussing how times that of
to prevent air. Thus, cold
transfer
occurs with
conversion of
and warm liquids
intravenous (water, sweat)
fluids are to the gaseous
very effective phase. The
in cooling first three
and warming mechanisms
the patient, are the most
respectively. important in
Radiation terms of heat
consists of loss, as well
heat transfer as for
resulting from rewarming
a temperature hypothermic
gradient, patients [13,
while evapo- 9, 14].
rative heat
 Various not only
methods have transfer heat
been across
employed to cutaneous
rewarm surfaces, but
patients and also create a
to prevent thermoneutral
perioperative microenvironm
hypothermia.
ent so that all
Active
external heat production
warming with goes to
both heating, restoring body
reflective and temperature.
convective air Thermoregulat
blan-kets, as ory
well as vasoconstrictio
radiant heat n, which
shields and separates and
fluid- and air- limits heat
circulat-ing transfer
warming between
blankets and peripheral skin
mattresses
and central
have been
tested and thermal
employed in compartments,
clinical limits the rate
practice [9, of rewarming
10, 12, 14, using forced air
15, 17, 19 [58].
21, 29, 42
53].
Other
Warming
Forced-Air Devices
Warming Neither
(Convective resistive
Air Blankets) heating using
Considerab electric
le evidence blankets nor
exists radi-ant
demonstrating
warmers
using infrared
the safety and radiation have
efficacy of become
forced-air important
warming
devices in both
preventing and
treating
hypothermia
and preventing
shivering
during the peri-
operative
period, as well
as with
accidental
hypothermia
(Fig-ures 29.6
and 29.7) [9,
12, 14, 35, 42,
5457]. If a
large enough
surface area
can be covered,
these devices Figure 29.6.
Convective
warming device. H YP
Upper body OTHE
RMIA
convective
IN T
(forced-air) RAU
warming device MA

and hose (Bair 449
Hugger Model
750 Warming
Unit, Arizant
Healthcare, Eden
Prairie, MN).
Heated air from
the warm-ing
unit inflates a
single-use
blanket. The
blanket design
contains a series
of hollow tubes
with rounded
upper surfaces
and flattened
lower surfaces
joined in a
parallel array.
Once inflated,
the blanket
directs heated air
onto the patient
through exit ports
in the blanket
undersurface.

Figure 29.7.
Convective
warming device.
The hypothermia
station con-sists
of a convective
warming unit
(Snuggle Warm)
and a fluid
warmer
(Hotline). The
convective
warming unit
draws ambient
room-
temperature air
through an
ultrafine glass
inlet filter.
Filtered air is
passed through a
0.2-m outlet
filter, heated, and
delivered through
a hose to the treatment of
disposable victims of
blanket. The accidental
fluid warmer hypothermia
heats water to a and during

42 C setpoint, trauma
and the warm resuscitation of
water is then already cold
circulated and exposed
through a patients [3, 59].
disposable set Grahn et al.
that has a sterile achieved
central lumen for impres-sive
IV fluid rewarming
administration results in
surrounded by an postoperative
outer layer
patients (46)
through which
and cold-
the warm water
stressed adults
circulates down
(60) by using a
one side and then
prototype
back up to the
heated reservoir, negative-
which prevents pressure
cool down in the warming
patient line. device.
There is a four- Subsequent
outlet power strip commercial
and an adjustable models did not
hose-tree arm show the same
(Smiths Medical effect [61, 62].
ASD, Rockland, Recently, Rein
MA). et al. [63]
showed that
locally applied
warm water
and pulsating
methods for negative
use during or pressure
after surgery prevented
[35]. They may hypothermia
play a larger during
role in the field laparotomy and
was superior
450 S oR heat to the core
E I D E AN D SM in patients
ITH requiring fluid
and blood
resuscitation.
to forced-air For example,

warming in 10 L of 40 C
terms of fluid given to a

maintaining 32 C patient
normothermia supplies 80
during kcal, which is
prolonged enough to
laparotomy. increase core
temperature in
a 70-kg patient
Fluid and
Blood by 1.4 C [64].
The thermal
Warmers stress of
Warm IV infusing large
fluids minimize volumes of
further heat room
loss while at temperature
the same time crystalloid and
transferring colloid or
significant inadequately
amounts of warmed blood
and blood
products can
result in temperature,
considerable
decreases in the greater
mean body the decrease
temperature [3, in body
14, 35]. The temperature.
larger the As well, the
gradient greater the
between the fluid
temperature of requirement
the infused relative to
fluid and core body weight,
the greater
the fall in
body
temperature.
The ability
of fluid and
blood warmers
to safely
deliver nor-
mothermic
fluids over a
wide range of
flows is limited
by sev-eral
factors
including
limited heat
transfer
capability of
mate-rials such
as plastic,
limited surface
area of the heat
exchange
mechanism,
inadequate heat
transfer of the
exchange
mecha-nism at
high flow rates,
and heat loss
after the IV
tubing exits the
warmer.
Improvements
in fluid warmer
design
including
higher set
points, greater
thermal
capacity, air
detection, and
line pressure
monitoring
allow the
clinician to
safely maintain
thermal
neutrality with
respect to fluid
management
over a wide
range of flows
(Figures 29.8 Use of
29.11) [6570]. effective

A
B

Figure 29.8. Rapid infusion fluid-

warming device (H1200, Smiths
Medical ASD, Inc, Rockland, MA).
The device consists of a heater that
warms water and circulates it through
a pump and a heat-exchange segment
with a central tube for water flow
(countercurrent heat exchange
technology). Fluid flows through the
outer sheath, which surrounds the
water core. (A) A pneumatic external
compressor automatically squeezes
the IV fluid or blood bag to increase
flow. Normothermic fluid delivery is
maintained at flows between 40 and

400 mL/min (20 C input), and at
flows between 40 and 300 mL/min

(10 C input). (B) The use of
ultrasonic air detection coupled with
automatic shutoff is a significant
safety improvement. (Avula RR,
Kramer R, Smith CE. Air detection
performance of the Level 1H-1200
fluid and blood warmer. Anesth Analg
2005;101:14136.)
H YPOTHERMIA IN T R AU M A 451

Temperature
Monitoring
The most reliable
temperature-
monitoring sites are
the distal
esophagus,
nasopharynx,
tympanic
membrane, and
pulmonary artery
(Table 29.5). These
sites come closest
to reflecting core
temperature that
Figure 29.9. Rapid
provides
infusion fluid warmer
approximately 80
device (FMS2000,
percent of thermal
Belmont Instrument
input to the
Corp., Billerica, MA).
hypothalamus.
This device uses
Core temperature
magnetic induction as
can be estimated
a heat source. An
with reasonable
integrated peristaltic
accuracy by using
pump eliminates the
intermediate sites
requirement for
such as sublingual
compression and
(oral), rectal, and
pressurization of the
bladder
fluid bag. Maximum
temperatures
flow is 500 mL/min.
except dur-ing
The device contains
extreme thermal
two air detectors, an
perturbations when
automatic air purge,
intermediate sites
and a line pressure
may lag behind
sensor. There is
core sites. Lag time
redundant air
is a function of
detection, automatic
both the mag-
air removal, and
nitude of heat
sensors to alert the
transferred and the
operator when the
time frame in
system is out of fluid,
which it is
or a line is obstructed.
accomplished. Lag
(Smith CE, Kabbara
time reflects
A, Kramer RP, Gill I.
restricted perfusion
A new IV fluid and
to specific body
blood warming
temperature-
system to prevent air
monitoring sites
embolism and
and/or imperfect
compartmental
sensor placement.
syndrome. Trauma
Care 2001;11(2):78
82.)
Distal
Esophagus
fluid-warming Because of its
devices permits proximity to the
more efficient
rewarming of heart, distal
hypothermic esophageal ther-
patients when mometry is a
combined with highly accurate
other methods measure of core
such as forced air temperature. The
[66]. thermistor is
contained within an
esophageal
stethoscope, which
is routinely used
for monitoring
heart and lung
sounds during
general anesthesia
in tracheally
intubated patients
(Fig-ure 29.12). If
the probe is not
placed distally,
temperature read-
ings may be
inaccurate. Distal
placement is
usually assured by
listening for the
loudest heart
sounds. Continuous
suction applied to a
nasogastric tube
will falsely lower
esophageal tem-
perature.

Nasopharyngeal
This site
usually correlates
well with other
centrally mea-sured
temperatures. A
Nasopharyngeal
temperature
exceeded

Figure 29.10. (A)

Pediatric in-line fluid
warmer disposable set
and heat-ing unit. The
disposable set is
attached close to the
patient to minimize
heat loss in the
patient line. Priming
volume is small (4
mL). (B) The
disposable set has
microporous
membranes that vent
air from crystal-loid
fluid. Air is released (Avula RR, Smith
through the side vents CE. Air venting and
of the set to minimize in-line intravenous
the risk of air fluid warming for
embolism (Buddy, pediatrics.
Belmont Instrument Anesthesiology
Corporation, 2005;102:1290)
Billerica, MA).
452 S oR E I D cabinet warmer load.
E AN D S MITH The warming
cabinet cannot be
used for blood.
(Raymond CJ, Kroll
A, Smith CE.
Warming crystalloid
fluid for intravenous
infusion: how
effective is a fluid
warming cabinet?
Anesth Analg.
2006:103:16056.)

tympanic
temperature during
rewarming on
cardiopulmonary
bypass (CPB),
which suggests that
this site better
reflects the brain
temperature [71].
Problems with this
site include the risk
of nasopharyngeal
bleeding.
Temperatures may
vary between
different probe
positions. This site
is relatively
contraindicated in
patients with severe
Figure 29.11. Fluid midface or basilar
warming cabinet skull fractures with
(Enthermics cribiform plate
Medical System,
disruption.
EC770L,
Menomonee Falls,
WI). The cabinet is
Pulmonary
Artery
warmed to 42 C by
The
using a low-heat-
pulmonary artery
density
(PA) catheter
electrothermal cable
contains a distal
array to provide
ther-mistor and is
even heating of used to monitor
injection fluids. The cardiac filling
stability of some pressures, stroke
solutions may vary volume, mixed
according to venous
temperature and oxygenation,
duration of storage. cardiac output,
Solution warm-up and other
time varies hemodynamic
depending on parameters. It is
too invasive to
use this site for
temperature Table 29.5:
measurement Temperature
alone. In the Monitoring Sites in
absence of pul- Order of
monary blood Authors
flow during CPB, Preference
PA temperature is
not accu-rate. Core

Distal esophagus
Nasopharynx
Tympanic membrane (ear)
Pulmonary artery

Modified from
Kabbara A, Smith
CE: Monitoring
temperature. In
Wilson WC,
Grande CM, Hoyt
DB, ed. Trauma:
Resuscitation,
Anesthesia, and
Critical Care. New
York: Taylor &
Francis Group,
2006. Reproduced
with permission.

Tympanic
Membrane (Ear)
The tympanic
membrane is 3.5
cm from the
hypothalamus, is
perfused by the
internal carotid
artery, and can be
readily monitored
using a well-
insulated
thermocouple
probe (ther-
mistor) adjacent to
the membrane
itself. Cerumen or
dried blood in the
aural canal can
result in a delayed
response time.
Tympanic
membrane probes
are
contraindicated in
patients with
cerebrospinal fluid
otorrhea and are
easily dislodged
dur-ing patient
movement and
transport.
Measures may be
inac-curate if the were sufficiently
ears are cold or in precise for routine
the presence of use. Indeed, the
otologic dis-ease. standard deviation
It is important to
of about 0.8 C
distinguish the
rather
cumbersome but
accurate method
of applying a
tympanic
thermistor probe
in the aural canal
[46] from the
simpler to use, but
less accurate
infrared aural
canal thermometer
[72]. Although
very feasible for
screening and
prehospital use Figure 29.12. Distal
esophageal
[73, 74], infrared
thermometry. 18 Fr
aural canal
esophageal stetho-
thermometers are
scope with 400 series
not considered
thermistor (Novamed,
appropriate for
Rye, NY). The
anesthesia and
stethoscope is a latex-
critical care use.
free single-use device
Measurement that continuously
from four measures core tem-
products using perature in tracheally
this technique intubated patients.
were compared The esophageal
with tympanic stethoscope is
thermistor mea- positioned at the point
surements from of maximal heart
the counterlateral sounds, and
ear during CPB temperature is
cooling [72]. displayed on an
None of the electronic monitor. A
infrared 9 Fr size is available
thermometers for pediatrics.
essential.
Advantages are
easy
indicated that accessibility,
familiarity, and
close to 70 noninvasive-ness.
Disadvantages
percent of the are related to
measurements inaccurate
readings due to
would span a noncompliance
or rapid mouth
range of 1.6 C breathing.
around the true
Rectum
thermistor value.
Rectal
Sublingual temperature was
Sublingual long considered
temperature is the gold
lower than core standard for
temperature by estimating core

about 0.5 C. temperature
Correct (especially in
placement of the
thermometer is children), and is

about 0.1 C
higher than core
temperature. ACCIDEN
Advantages are TA L H Y P O T
easy accessibility, HERMIA
low cost, and Definitions and
accurate readings.
Physiologic
Because the rec-
tum is a cavity, it Consequences
can retain heat Accidental
longer than other hypothermia has
temperature sites. been defined as an
When a patients unintentional
temperature is decrease in core
rising or falling temperature below

rapidly, the 35 C. The
temperature in the thermoregula-tory
rectum can lag capacity for
behind by as compensation will
much as an hour. vary from person
This may be to person based on
age, health status,
because the and intake of
rectum contains drugs and alcohol
no thermore- (Tables 29.1 and
ceptors and thus is 29.2) [30, 59, 75,
heated or cooled 76]. For the same
as an effect of cold expo-sure the
hypothalamic thermoregulatory
control, rather capacity of the
than in response person will
determine when
to it. Other hypothermia sets
possible causes of in or the person
inaccurate rectal merely remains
readings are cold stressed
related to the (feeling cold,
insulating effect shivering,
of fecal matter in vasoconstricted,
the rectum and the with body
heat produced by temperature above

coliform bacteria. 35 C) [30, 60].
The classic
distinction
Bladder between mild

Bladder (35 C32 C),

temperature can be moder-ate (32

measured by an C28 C), and

indwelling urinary severe (<28 C)
catheter containing accidental
a thermistor. If the
hypothermia is
still used [30,
patients uri-nary 59]. However,
catheter does not the new
guidelines from
have a thermistor the Inter-national
attached, it has to Liaison
be changed to one Committee of
Resuscitation
that does. Low (ILCOR), which
urinary flow may among others
decrease the ability includes the
European
of this site to Resuscitation
reliably estimate Council (ERC)
core temperature and the American
Heart Association
(e.g., shock, renal (AHA), uses less
failure). Open
than 30 C as the
pelvic and lower cutoff point to
abdominal trauma define severe
hypothermia [36,
may falsely lower 77].
temperature Prolonged
readings from this exposure to
site. temperatures
outside the TNZ H
causes hypothermia Y
P
even in mild and O
hot climates. T
H
Hence, accidental E
hypothermia R
M
should not be IA
considered an IN
arctic or wilderness T
R
problem. Rather, it A
can occur in U
M
healthy persons A
exposed to ambient

air temperatures, 4
5
precipitation, and 3
wind

chill despite the

initial protection by
isolation and
thermoregu-latory
compensation
(increased heat
production).
Immersion or
submersion in cold
water accelerates
the onset of
hypother-mia [30,
76, 78]. With
intoxication and
illness,
hypothermia is well
described in urban
and warm
surroundings [30,
76, 78]. Hence,
accidental
hypothermia
should always be a
differential
diagnosis in
obtunded and
collapsed patients.
The diagnosis
mandates only one
single measure of
decreased core
tempera-ture using
a low-read
thermometer.
Predisposing
factors for
involuntary cooling
of the body and the
thermoregulative
countermeasures
are shown in Tables
29.1 and 29.2 and
Figures 29.2 to
29.4. General
symptoms seen
with progressive
accidental
hypothermia are
outlined in Fig-ure tical and
29.13 (see also therapeutic point of
color plate after p. view [36, 7982].
294). From a thera- Still, the merit is
peutic point of evident based on
view, it is multiple successful
important to cases of good
differentiate neurologic
between outcome.
mild/moderate
versus severe
hypothermia [30,
Treatment
36], between
Options in
arrested versus
Patients with
nonarrested
Mild,
hypothermic
Moderate, or
victims, and
Severe
between
Accidental
asphyxiated and
Hypothermia
nonasphyxiated
with Intact
hypothermic arrest
Circulation
[36, 77].
In severe The degree of
hypothermia, the hypothermia will
initial slowing of determine the most
the heart and appropriate
supraventricular rewarming
arrhythmias give techniques. In mild
way to ventricular hypothermia,
fibrillation (VF) transferring the
and, finally, patient from the
asystole [30, 59]. cold environment
The respiratory rate to warm and
slows dramatically, protected sur-
and the roundings,
unconscious patient removing cold and
with dilated pupils wet clothes, drying
may appear dead. the body sur-face,
The distinction and blanket
between a dead coverage is
person and a sufficient in most
severely cases [2, 30, 36,
hypothermic 59]. Under these
patient becomes circumstances, the
problematic. bodys own heat
Therefore, the production will
general consensus reverse the low
is that no temperature
hypothermic (passive external
patient should be rewarming). If the
pronounced dead patient is very
before warm and uncomfortable or
dead [2, 30, 36, unable to
77]. An aggressive spontaneously
approach to reverse the
rewarming is hypothermia,
indicated. This external active
approach with rewarming is
prolonged indicated (Table
cardiopulmonary 29.6).
resuscitation (CPR) In moderate
and use of CPB is hypothermia, active
resource intensive external rewarming
and complicated, is indicated.
both from a logis- Forced-air
warming is have been
probably the most described [2, 30,
effective and 36, 56, 57, 59, 75,
practical method 76, 8385] and rec-
and can also be ommended for
used in severe moderate and
hypother-mia, as severe hypothermia
long as there is an (Table 29.6).
intact circulation In severe
(pulse present) [30, hypothermia, the
36, 56, 57, 59]. pulse will become
Other external re- slow, irregular, and
warming methods more small-volume
include warm- and blood pressure
water baths, heated may be unrecord-
blankets, heat able [30, 59, 76]. In
lamps, heat packs, such patients,
and reflective endotracheal
blankets. Infusion intubation and
of warm IV fluids other
is important, and manipulations at
methods such as the scene, during
gastric, bladder, transport, or on
peritoneal, and arrival
pleural lavage,
454 S oR E I D E AN D S MITH

COLD INJURY

EARLY LATE THAW

Extracellular +/ intracellular
Inceased
CELLULAR EFFECTS H2O crystallization extracellular fluid
OF COLD Cell death
Cellular dysfunction
Membrane
damage SYSTEMIC EFFECTS
Water leaves OF COLD
cells
+
++ Electrolyte
imbalance Cognitive dysfunction,
delirium, aphasia
Modified protein amnesia, coma
structures
J waves,
decreased contractility,
bradycardia,
arrhythmia
THERMOREGULATORY
RESPONSE V/Q mismatch

Hypertension, Rewarming
tachycardia Shock
shock
Ileus
Cold diuresis,
Bladder atony renal failure
Shivering
Peripheral
vasoconstriction Rhabdomyolysis Bullae

TISSUE EFFECTS
OF COLD
Stasis Neuropathy

Gangrene
Endothelial
injury
Interstitial edema

Lactic acidosis
Hemoconcentration

Thrombosis

Vascular insufficiency

Figure 29.13. Cold-induced injuries such as hypothermia and frostbite lead to thermoregulatory response (e.g., shivering and increased
sympathetic activity), cellular and tissue effects (e.g., membrane damage, electrolyte imbalance, endothelial injury, and thrombosis) and
systemic effects (e.g., shock, arrhythmia, and neuromuscular dysfunction). Reproduced with permission from reference 30.
H YPOTHERMIA IN T R AU M A 455
Table 29.6: Rewarming Methods and Rewarming Rates with Different Alternatives

Rewarming Rate
Category Methods Comments ( C/hr)
Passive external Blankets Including head and neck, reduces 0.54
evaporative heat loss, unsuccessful if there
is loss of shivering
Humidifier-inspired air Including head and neck, reduces Variable
evaporative heat loss, unsuccessful if there
is loss of shivering
Active external Forced-heated air Risk of temperature afterdrop and 12.5
rewarming hypotension
Warm blankets Risks of burns, temperature afterdrop, and Variable
rewarming hypotension
Warm-water immersion Difficult to monitor patient, risk of 24
temperature afterdrop and rewarming
hypotension

Active internal Warm (42 C) humidified air Low heat transport capacity 0.51.2

Warm (42 C) intravenous fluids Especially useful in the resuscitation of Variable
hypothermic trauma victims, rapid
infusion maximizes heat delivery
Body cavity lavage with warm fluid (gastric, Limited data, risk of mucosal injury, risk of Variable
bladder, colon, pleural, peritoneal) aspiration with gastric lavage
Extracorporeal Hemodialysis and hemofiltration Widely available, rapid initiation, requires 23
adequate blood pressure
Continuous arteriovenous rewarming Rapid initiation, trained perfusionist not 34
required, less available, requires adequate
blood pressure
Cardiopulmonary bypass Provides full circulatory support, allows 710
oxygenation, less available, requires
trained perfusionist, delays in initiation

Reproduced with permission from reference 59.

unconscious patient provided there is a perfusing rhythm based
on the fol-lowing reports. In a randomized controlled trial of
to the hospital may provoke VF [30, 36, 79, 83]. Hence, gen-tle hypothermic
handling is important. If signs of life are present (palpable
carotid artery pulse, QRS complexes on the electrocardiogram
(ECG), spontaneous breathing for at least 1 min), the combina-
tion of rapid external/internal rewarming (Table 29.6), warm
humidified oxygen by mask, and warm IV fluids to counter-act
the expansion of the vascular bed and to replace the fluids lost
during cooling is sufficient [30, 36, 83]. A definitive air-way
may be necessary. Arrhythmias other than VF will revert
spontaneously with normalization of temperature. In otherwise
healthy patients, the prognosis is excellent [7, 30]. In moderate
and severe hypothermia with an intact circulation, the prog-
nosis largely depends on the underlying diseases and causes of
hypothermia [30, 59, 75, 76, 78]. Reported in-hospital mortal-
ity varies from 10 to 40 percent, with numbers approximating
50 percent in those with severe underlying cardiopulmonary
diseases.

At present, one rewarming method cannot be recom-

mended over another in terms of outcome and efficacy. How-
ever, from a practical and safety point of view, we believe
forced-air warming is a reasonable choice, even in the
 perature to prevent an uncontrolled drop in temperature and to
evaluate the efficacy of rewarming. Arrhythmias and hypoten-
patients with an average core temperature of 28.8 C, forced-air sion may occur due to peripheral vasodilatation, as well as from

warming increased core temperature by about 2.4 C/hr vs. 1.4 cool blood returning to the central circulation (afterdrop) [2, 30,
C/hr in controls [55]. Both groups of patients received IV fluids 36, 86]. There is an increased need for intravenous fluids during

warmed to 38 C as well as warmed, humidified oxygen at 40
the rewarming period.
C by inhalation. Koller et al. [56] reported the use of forced-air Accidental hypothermia may be associated with local cold-
induced injuries [30]. These are most commonly seen in the
warming in five patients with core temperature of less than 30 extremities. They are classified as superficial (clear blisters) or
C. The outcome of all five patients was good without neu- deep (hemorrhagic blisters) [30]. If refreezing is not a problem,
rologic sequelae. Core temperature increased by approximately

local rewarming during transport should be started. However,
1 C/hr without any cardiac arrhythmias or core temperature not by rubbing as this may worsen the tissue damage. Fur-ther
afterdrop. It is important to continuously monitor core tem- management beyond rapid rewarming in hot-water baths
4 5 6 S oR E I D E A N D S M I T H rewarmed after immersion (as opposed to after drowning or
avalanche) was good, with reported rates of intact survivors up
to 60 to 70 percent [7, 36, 7982].

(40 C42 C) is still controversial [30]. Independent of
the cho-sen approach, the need for prolonged hospital
stay and repeated surgical procedures is frequent. Treatment Options in Hypothermic Cardiac
Arrest Victims with a History of Asphyxia
Treatment Options in Hypothermic Cardiac At stated above, the association of hypothermia with asphyxia
Arrest Victims without a History of Asphyxia carries a poor prognosis. Because the prehospital clinical
picture may be unclear, and prehospital signs such as dilated
In hypothermic cardiac arrest victims, CPR should be com-
pupils and asystole have no prognostic value, every effort
menced by using the same ventilation and compression
ratios/rates as in normothermic patients (30:2; rate, 100/min) should be made to start immediate and adequate CPR [36]. In
[36]. The general stiffness of the whole body will make CPR drowning cases, this is especially important. Even imperfect
more complicated and a strange experience for the rescuer. and simple bystander CPR may bring the patient back to life.
There is a general consensus that vasoactive drugs and defibril- While submersion implies that the whole body has
been underwater, immersion only means being covered
lation are less effective if the core temperature is less than 30 in water/
C. However, a trade-off between this concern and the provision
of rapid, effective therapy to reverse VF has been made in
recent international guidelines by stating that if VF/VT
persists after three shocks, delay further defibrillation attempts

until core temperature is above 30 C [36]. The general
consensus for drug therapy is to withhold epinephrine and other

drugs such as amiodarone until core temperature reaches 30 C.
Endotra-cheal intubation is indicated in hypothermic cardiac
arrest not only to secure an airway and to ventilate, but also

rewarm by using warmed (maximum, 42 C) humidified
oxygen/air [36].
Survivals after hours of resuscitation and weeks of
inten-sive care have been reported even in patients with

profound (<20 C) hypothermia [80]. Hence, in the absence
of obvious lethal injuries or a completely frozen body
making CPR impos-sible, the patient should be transported
with ongoing CPR to a hospital capable of providing rapid
invasive rewarming through the use of CPB (Table 29.6)
[36, 7982]. The management of such patients will require
close cooperation between personnel specialized in
cardiothoracic surgery, perfusion, cardiac anes-thesia, and
intensive care. Issues such as optimization of tis-sue
perfusion, prevention of ischemia, and knowledge of the
pathophysiology of reperfusion and microcirculation flow
dys-function need to be addressed but are outside the scope
of this chapter.
The outcome in these patients not only depends on the
temperature at the start of the resuscitation, but on the cause of
the hypothermia and underlying diseases. When analyzing the
outcome of hypothermic cardiac arrest victims rewarmed with
extracorporeal circulation, the critical factor has been found to
be the presence or absence of asphyxia prior to the onset of
hypothermia. For example, the overall prognosis in victims

fluid. Hypothermia will develop with both immersion and sub-
mersion [78]. If the airway has been kept clear and over the
water in immersed victims, hypothermia and subsequent car-
diac arrest are not necessarily associated with asphyxia
(primary hypothermia). In submersion, the situation is more
compli-cated as the general rule is that associated asphyxia and
cardiac arrest carry a poor prognosis even if hypothermia
develops. If the submersion occurs in icy water, thereby
inducing rapid cool-ing of the brain, the situation is quite
different. Intact survivors have been described after up to 60-
min submersion periods, especially in children [36].
CPR and advanced life support procedures in victims
of drowning should follow the procedures presented for
nonas-phyxiated hypothermic cardiac arrest victims
above. Postresus-citation, comatose survivors should
probably be kept mildly hypothermic (32 C34 C) and
mechanically ventilated for at least 24 hours [87].
Avalanche victims constitute a special group [36, 56, 57,
81, 82, 88, 89]. Blunt trauma is the reason for death in up to
one third of avalanche victims, and early asphyxiation is also
com-mon [88, 89]. Hypothermia is rarely the mechanism of
death. It may become an important mechanism in those buried
with an air pocket that allows respiration initially. Survival data
from the European Alps have shown that the probability for
survival in completely-buried victims fall rapidly from 90
percent after 15 min burial time to 30 percent after 30 min [88,
89]. Survival after 90 min is low. Triage and field management
are difficult. In the initial half hour, the focus should be on
rapid extrication and immediate airway management and CPR
in lifeless victims to counteract asphyxia. With longer burial
times, treatment of hypothermia becomes more important.
Table 29.7: An Alternative Proposal for
Classification of Hypothermia in the Trauma Patient
General Medical Proposed Trauma
Classification Classification
Category C Class
Mild 3532 I 3635 measurement (core vs. intermediate site, thermocouple
II
Moderate 3228 III
Severe 28 IV
Reproduced with permission from reference 2.
Nonintended hypothermia in trauma victims is still a com-
mon problem and occurs early during the resuscitative phase
[3]. Due to the overall more negative effects (increased
bleeding and immunosuppression) of accidental hypothermia in
trauma patients, the classic cutoff points have been redefined
for the trauma population [1, 3], such that mild hypothermia
corre-sponds to a core temperature between 34 C and 35.9 C;
mod-erate hypothermia, 32 C to 33.9 C; and severe
hypothermia, less than 32 C. An alternative classification of
hypothermia can be used with four classes (IIV), as shown in
Table 29.7.
Hence, gentle extrica-tion, ECG, and core temperature
monitoring is mandatory. The trachea of lifeless victims should
be intubated, and if the core temperature is less than 32 C,
those found with an air pocket and clear airways should be
transported with ongoing CPR to a hospital able to provide
extracorporeal rewarming [36, 88, 89].
T R A U M A - A S S O C I AT E D H Y P O T H E R M I A
Definitions, Predisposing Factors, and Incidence
Despite decades of ongoing discussion and lab research on the
possible protective effects of hypothermia in trauma patients [2,
5], the development of hypothermia is still considered
detrimental [13]. Much discussion has centered on whether
hypothermia is just a result of the shocked state itself, with low
perfusion causing reduced metabolism and diminished heat
production, or an imposed complication with an independent
negative influence on prognosis. In their review of this topic,
Hildebrand et al. [1] concluded that accidental hypothermia in
trauma victims is a very different situation from controlled,
induced hypothermia (therapeutic) in trauma patients. Labora-
tory research has shown beneficial effects of induced hypother-
mia during hemorrhagic shock despite the fact that hypother-
mia per se increases the bleeding tendency. Hypothermia has a
definite anti-inflammatory effect, which can be used to ame-
liorate reperfusion injuries in various organs. While induced
hypothermia with shivering prevention preserves body reserves
of high-energy substrates, accidental hypothermia in trauma
patients causes physiologic stress and depletion of the same
sub-strates, resulting in both increased morbidity and mortality
[1].
While the incidence of hypothermia in trauma victims has
been widely studied, there is still a paucity of data when it
comes to comparing different treatment algorithms and
rewarming techniques in trauma patients. The noted differences
in inci-dences may be due to differences in (1) the trauma
system and population itself (urban vs. rural, blunt injury vs.
penetrating;
(2) timing of temperature measurements (prehospital vs.
C emer-gency department vs. operating room vs. intensive
care unit [ICU]); (3) technique of temperature
3432 vs. infrared device); and (4) differences in trauma
systems (thermal prevention methods vs. none, warmed
3228 IV fluids vs. unwarmed, immediate vs. delayed fluid
28 resuscitation).
In one of the few prehospital studies, Helm et al. [73]
found that almost every second patient was hypothermic.
Entrapped patients were at higher risk (98% vs. 35%; P <
0.001), as were patients older than 65 years (P < 0.001).
Clinical symptoms of hypothermia such as shivering were
only noted in 4 percent. Little et al. [90, 91] also detected a
lack of shivering response to hypothermia in traumatized
patients immediately after injury. The absence of shivering
to compensate for the fall in core temperature is likely due
to impaired thermoregulation after injury [1, 73, 90]. In
animal research, the threshold hypotha-lamic temperature
for onset of shivering was 34.8 to 36.4 C in control
animals, whereas after injury, the threshold was low-ered so
that either no shivering occurred, or only slight shiver-ing
was observed at about 31 C [92]. A similar impairment in
the threshold for vasoconstriction may also occur after
trauma. Possible mechanisms include reduced tissue
oxygenation due to shock, central noradrenergic inhibition,
central effects of hypotension and hypovolemia, and
decrease in baroreceptor input to the brain [9094].
Using a tympanic infrared thermometer technique, Watts et
al. [74] showed that more than 60 percent of their trauma
H YPOTH E RMIA IN T RAU M A 4
57
patients transported with air and ground ambulances had a
subnormal temperature at initial assessment. Fewer than 5
per-cent, however, had a temperature below 34 C.
Interestingly, there were no seasonal differences. In a study
from conflict zones in Southeast Asia, Husum et al. [95]
found that basic prehospital interventions to reduce heat loss
were able to sig-nificantly reduce the frequency of
hypothermia despite overall long transport times of six to
seven hours.
Studies from the emergency department (ED) also sup-port
the notion that hypothermia is prevalent. Luna et al. [96] found
that that about 66 percent of tracheally intubated trauma
patients arrived in the ED hypothermic. Hypothermia during
the initial phase in the hospital was associated with both the
severity of injury, number of transfusions needed, and time
spent prehospital and in the ED. The overall incidence of
admis-sion hypothermia, defined as temperature 35 C, was 5
per-cent in a study using data from a statewide trauma registry
in Pennsylvania (n = 38,520 patients) [97]. Even after adjust-
ment for other factors, admission hypothermia was associated
with 3-fold increased odds ratio for fatal outcome. Periopera-
tive hypothermia has been shown to occur in almost 50 percent
of trauma patients requiring early surgery (Figure 29.14). In a
recent study of 2,848 combat victims from Iraq [98], 18 percent
of the victims were hypothermic (<36 C) at arrival in the Com-
bat Support Hospital. However, only 0.2 percent was severely
hypothermic (<32 C) and 2% had a temperature between 32
and 34 C (moderate hypothermia). Both penetrating injury
mechanism, a Glasgow Coma Scale score less than 8, and
shock defined as a systolic blood pressure (SBP) lower than 90
mmHg were independent predictors of hypothermia on arrival.
Analyzing 38,550 trauma patients aged 18 to 55 years
from the National Trauma Data Bank (American College
of Sur-geons), Shafi et al. [99] found an 8.5 percent
incidence of hypothermia at arrival in the ED.
Hypothermic patients had the same age and sex
distribution as the normothermic patients, but in general
were more severely injured.
If not present at arrival, hypothermia may develop and
worsen during the stay in the ED and OR (Figure 29.14). The
etiology, predisposing factors, and pathophysiology are the
same as for other major surgery patients (Tables 29.129.3).
Incidence of Hypothermia
50
40
Patients
30
20
% of
10
0
Preop Intraop Final
Figure 29.14. Incidence of hypothermia (<36 C) in 660 trauma patients
requiring surgery within 24 hours of admission to MetroHealth Medi-
cal Center, Cleveland, Ohio. Preop, preoperative, intraop, Society of Anes-thesiologists Annual Meeting, Sept, 2004. Reproduced
intraoperative. Presented at MetroHealth Research Exposition and Ohio with permission.
458 S oR E I D E AN D S MITH detrimental in severely traumatized patients. Hence, every
measure should be taken to counteract a fall in body
temperature in trauma patients, both prior to and after
During initial resuscitation and surgical procedures, arrival at the hospital [13].
exposure of the patient, immobilization, use of
anesthesia, combined with suboptimal thermal protection
will soon render the trauma patient hypothermic.
Unfortunately, despite everything that has been written
on the subject there is still a distinct impres-sion that
thermal management of trauma patients is suboptimal [3,
4].

Clinical Implications, Prevention, and

Rewarming Options
The negative clinical consequences of hypothermia in
trauma victims are well-defined [13], and particularly
linked to coag-ulopathy and immunosuppression (Table
29.3). The critical core temperature for onset of

coagulopathy appears to be 34 C, at which level the
enzymatic activity and platelet function fall significantly
[100]. Older studies showed no trauma survivors with

temperatures below 32 C [101]. Newer data from the large
North-American National Trauma Data Bank do not support
the notion that the overall prognosis in patients with severe
hypothermia is dismal [102].
Prevention is always better than treatment, including dur-
ing intrahospital transport [103]. Comparing trauma patients in
need of massive transfusion (>50 units of packed red blood
cells) during two time periods in the late 1980s and early 1990s,
Cinat et al. [104] found that refractory hypothermia, severe
acidosis, and prolonged hypotension were factors linked to poor
outcome. They concluded that the noted increase in sur-vival
from 16 to 45 percent during the ten-year period studied most
likely was due to more efficient rewarming, aggressive
correction of coagulopathy, and improved application of dam-
age control surgery principles. Perioperative hypothermia and
hypothermia on arrival to the ICU or during the first ICU hour
should always be considered a danger sign.
More recent studies have shown the same correlation
between hypothermia and worsened outcome. Two recent
North-American National Trauma Data Bank reviews [99,
102] found that after adjusting for age, sex, mechanism, and

severity of injury, hypothermia (<35 C) on arrival to the ED
was an independent predictor of death (odds ratio 1.19 [95%
CI 1.05 1.35; P = 0.008]). Not surprisingly, the incidence
of infections overall, pneumonia, renal failure, and adult
respiratory distress syndrome (ARDS) were all significantly
higher in hypothermic patients. In cohort studies using
multivariate analysis on retro-spective data, there will
always be a question whether the sta-tistical association
found also implies a causal link. Both young (<18 years)
and old (>55 years) patients were excluded, and information
on prehospital time and thermal management was not
present. Further, in the study on the 2004 National Trauma
Data Bank [102] the mortality remained constant in patients

below 32 C. The fact that almost 60 percent of the patients

with a temperature below 32 C survived emphasizes that, in
modern trauma systems, a low temperature should not be
con-sidered a sign of futility of care. More data on the
subgroup of trauma survivors with a very low temperature is
needed. In conclusion, both these large cohort studies
support the notion that the development of hypothermia is

In one of the very few studies of prehospital intervention to
maintain normothermia in trauma victims, Watts et al. [74]
found that the use of chemical hot packs (Hot Cycle 1; Sig-nal
Manufacturing Corporation, Fairfield, CA) increased body
temperature during transport. Neither passive rewarming and
reflective blankets nor warmed IV fluids alone caused the same
increase in temperature. Although the study numbers were
small, the results suggest that hypothermia in trauma victims is
undertreated, and further research is required on prehospital
thermal management.
Using a laboratory model to simulate trauma patients, Ittner
et al. [105] compared resistive heating blankets with a
convective air-warming device. The convective warming was
more effec-tive. Kober et al. [106, 107] compared resistive
heating blankets and wool blankets during ambulance
transports of trauma vic-tims. Use of the resistive heating
blankets both caused more thermal comfort, less fall in oral and
tympanic measured tem-perature, and a better pulse oximeter
signal. The conclusion of the authors [105107] that such
devices should be made avail-able in all ambulances is
hampered by many practical, logistical, and financial barriers.
Still, prevention of early hypothermia in the prehospital phase
should be emphasized. This also includes the judicious use of
IV Fluids [108], as use of cold fluids is a very effective way of
inadvertently cooling trauma patients [87, 109].
In-hospital, convective warming devices are very useful in
a wide variety of locations (ED, OR, ICU, postanesthesia care
unit), and if a large enough surface area can be covered, these
devices create a thermoneutral microenvironment such that all
heat production goes to restoring core temperature [4, 35, 65,
67, 68, 110]. It is recognized that it may be somewhat dif-ficult
to apply these devices to the trauma patient in the ED because
of the requirement for patient exposure. In the operat-ing room,
particularly with multiple injuries, there is very little surface
area available for the application of the upper-, lower-, or
whole-body convective warming blanket. In these instances, an
underbody forced-air or resistive heating blanket can be of
significant benefit [14, 35, 44, 111], as can radiant heaters [35].
Other warming methods are also available in trauma
patients (Tables 29.629.8). Heated humidification of the
breathing circuit will prevent respiratory-gas-related heat
loss and can add heat to the patient. Delivery of warm,
humidi-fied gas has been shown to increase core
temperature by 0.5 C to 0.65 C per hour in injured,
hypothermic patients [112, 113], and should be used as an
integrated part of a combined approach to treat or prevent
hypothermia [35].
Although mostly used for accidental hypothermia
patients (see Accidental Hypothermia), active, internal
rewarming (Tables 29.6 and 29.8) restores normothermia at
a faster rate than surface methods and has been associated
with more rapid normalization of cardiac output and ECG,
and a decreased risk of rewarming shock in trauma-
associated severe hypothermia [64, 114, 115]. These
methods of core rewarming are generally appropriate for
severely hypothermic patients, but may also be useful for
moderately hypothermic patients (3234 C) with
cardiovascular instability.
CPB (Tables 29.6 and 29.8) is the most effective means of
rewarming severely hypothermic patients, but requires sys-
temic heparinization [2, 3, 30, 59, 116]. Relative contraindica-
tions to CPB include asphyxia, severe traumatic injury (risk of
 H YPOTH E RMIA IN T RAU M A 459

Table 29.8: Suggested Management of Different Levels of Hypothermia in Trauma Victims

Hypothermia Type/Class
Mild Moderate Severe
Phase of Care Class I Class II Class III Class IV

Prehospital/emergency Standard measures Active external warming Extracorporeal measures Extracorporeal measures
department/critical care active external warming
unit

Intraoperative Standard measures Active internal warming Extracorporeal measures Extracorporeal measures
active external warming (intracavitary irrigation) intracavitary intracavitary
methods methods
Permissibility of further Completion of definitive Damage control Damage control Damage control
surgery? surgery Consider DHCA

Standard measures to be instituted in all serious trauma patients encompass but are not limited to measures recognized as passive external
methods (warm environment, blankets, covers), warmed intravenous fluids, warmed inspired gases if intubated, convective warming blankets.
Extracarporeal methods to be utilized with appropriate personnel and institutional support: continuous artenovenous rewarming, venovenous
rewarming with centrifugal vortex pump, arteriovenous rewarming with centrifugal vortex pump, standard cardiopulmonary bypass, hemodialysis
circuits with heated dialysate.
DHCA, deep hypothermic circulatory arrest (only with severe injuries and appropriate support). Reproduced with permission from reference 2.
charge was not significantly different between groups (66% sur-
vival with CAVR vs. 50% with standard rewarming). This study

bleeding), and greatly elevated potassium levels (>10

mmol/L). Peritoneal or pleural lavage with heated
crystalloid at an exchange rate of 6 L/min may increase

core temperature at a rate of 2 C to 3 C per hour, and
has been shown to be beneficial in patients sustaining
environmental or exposure hypothermia [2, 3, 30, 59,
84].
Another technique involves the connection of a percuta-
neously placed femoral arterial line to a counter-current
fluid warmer (Tables 29.6 and 29.8) [64, 114, 115]. The
patients blood volume flows through the warmer and
returns to the patient by large-bore venous tubing so a
fistula is created through the heating warmer (Figure 29.15).
This technique, known as continuous arteriovenous
rewarming (CAVR), has been shown to rapidly rewarm
mildly hypothermic patients. In the initial experience of 16

patients treated with CAVR, core rewarming to 35 C was

accomplished in 39 minutes and to 36 C in 66 minutes
[114]. Advantages of CAVR include no requirement for
heparinization, rapid reversal of hypothermia, decreased
total fluid requirements, decreased organ failure, and
decreased length of ICU stay. The CAVR technique
provided a continuous transfusion of heat to the patient as
long as systolic blood pressure was more than 80 mmHg.
The risks of CAVR consist mainly of those related to
percutaneous cannulation of the femoral vessels [114, 115].
There are very few randomized, controlled studies of
rewarming trauma patients. Gentillelo et al. [115] compared
CAVR with standard rewarming in a randomized, prospective
trial of 57 trauma patients arriving in the ICU hypothermic

(core temperature 34.5 C). There was a marked decrease in
fluid requirement, a significantly faster rewarming rate, and
lower early mortality in patients receiving CAVR (7% with
CAVR vs. 43% with standard rewarming), but survival to dis-
 Figure 29.15. Schematic description of the continous arteriovenous
rewarming (CAVR) device that uses percutaneously placed femoral
arte-rial and venous catheters and the patients own blood pressure
to create an arteriovenous fistula that diverts a portion of the
cardiac output through a compact, heparin-bonded heat exchanger.
Reproduced with permission from reference 114.
460 S oR E I D E AN D S MITH the ED. It is recognized, however, that clotting studies done at
normal body temperature in the laboratory will not confirm
hypothermic coagulopathy [100, 122, 123]. Using
illustrates the problems with such studies and how short-term thromboelastography adjusted to core body temperature, and
effects may be deleted by later problems in the ICU. Still, the prothrombin time (PT), activated par-tial thromboplastin times
study supports the notion that hypothermia should be treated (aPTTs), and platelet activity mea-surement in 112 consecutive
aggressively in trauma patients. The methods used (Tables 29.6 adult trauma patients, Watts et al. [100] found that a core
and 29.8) will vary with the circumstances and the experience
temperature of less than 34 C was the critical point at which
and available resources of the local trauma team. both coagulation enzyme activity and platelet function
decreased significantly. Fibrinolysis was not affected by a drop
Damage Control Surgery and ICU Treatment
in temperature. Patients with a temperature greater than 34.0 C
actually demonstrated hypercoagulobility.
The studies of Cinat et al. [104] and Gentillo et al. [115]
point to some of the same problems in trauma patients: that In their recent review of massive transfusion and
injury severity, hemorrhagic shock, resuscitation with fluids coagulopa-thy, Hardy et al. [124] concluded that maintenance
and blood products, coagulopathy, and hypothermia are of normo-thermia and correction of low hemoglobin should be
linked in a way that make it hard to differentiate the effects con-sidered basic, simple, and effective strategies to avoid
of injury from the effects of treatment [3, 65, 67, 68, 99, further bleeding. Rewarming is a first-line intervention in
117119]. Importantly, the deleterious effects of shock and diffuse bleed-ing situations. In situations with diffuse bleeding,
hypothermia on hemodynamic parameters and coagulation restoration of a critical red blood cell mass (hemoglobin, 910
are additive. This has led to the concept of damage control g/dL), platelet count (>75,000100,000 cells/mm [3]), PT (<1.5
surgery [2, 117, 119]. Hypothermia of less than 34 C
times nor-
together with acidosis (pH <7.10) and clini-cal diffuse
bleeding (coagulopathy) are recognized as the lethal triad
or bloody vicious cycle. These criteria are now used to
mark the limits for the tolerance of the patient for definitive
surgical control and repair. This applies both for laparotomy,
thoracotomy, and orthopedic surgery. Instead, an abbrevi-
ated approach to stop bleeding (packing) and prevent
ongo-ing contamination is sought. The patient is transported
to the ICU for rewarming, hemodynamic optimization, and
reversal of coagulopathy.
Traumatic coagulopathy is a syndrome of diffuse bleeding
from mucosal, serosal, and wound surfaces, as well as vascular
sites, associated with serious injury, hypothermia, acidosis, and
hemodilution [120]. Brohi et al. [121] used laboratory tests to
define the presence of early coagulopathy in 1,088 trauma
patients. They found that nearly one quarter of their patients
arrived in the ED with an established coagulopathy and linked
this to tissue injury and release of various factors. The
incidence of coagulopathy increased with increasing injury
severity score (ISS), as did mortality. The authors did not find a
significant cor-relation with prehospital fluid therapy and
concluded that early laboratory clotting tests should be
mandatory in all patients with multiple injuries upon arrival in

mal), International Normalized Ratio (INR; <1.5), and fibrino-
gen level (>80100 mg/dL) is important to make a large clot
for-mation possible. The hemostatic agent recombinant
activated factor VII (rFVIIa) has come into common use in
such criti-cal bleeding situations [118, 125]. While the efficacy
of rFVIIa depends on a pH higher than 7.1, it retains a normal
activity in the presence of hypothermia [125].
S U M M AR YAN D C O N C LU S I O N S
Hypothermia as a complication of major surgery and anes-
thesia is well known to the anesthesiologist. Life-threatening
hypothermia without trauma may also develop (accidental
hypothermia). Hypothermia often complicates the manage-
ment of patients with blunt or penetrating trauma and is asso-
ciated with increased morbidity and mortality. Early control of
bleeding and prevention of further heat loss are key factors to
avoid the lethal triad of hypothermia, acidosis, and coagulopa-
thy. In the middle of the stressful trauma resuscitation situation
it is important for the anesthesiologist to use his or her experi-
ence from major surgery and pay close attention to temperature
management in trauma patients.
M U LT I P L E C H O I C E Q U E S T I O N S
The most reliable temperature-monitoring sites are the
dis-tal esophagus, nasopharynx, and pulmonary
artery.
True
False
In humans, the core temperature remains stable within a
narrow temperature range despite large variations in
envi-ronmental conditions.
True
False
Regarding rewarming and maintaining normothermia
methods and equipment:
Conduction represents heat transfer through air that is
in contact with the body, and its efficiency is
mostly deter-mined by air velocity.
Convective heat transfer implies direct contact between
two objects and their characteristics.
Commercial rewarming equipment (e.g., convective
forced-air, fluid warmer) are generally not
effective in preventing perioperative hypothermia.
Evaporative heat transfer occurs with conversion of liq-
uids (water, sweat) to the gaseous phase.
Identify the correct statement regarding side effects of
peri-operative hypothermia.
Decreases
in core temperatures to between 34 C and
36 C have not been associated with a significant
increase in complications such as cardiac events
(myocardial ischemia, ventricular tachycardia).

Decreases in core temperatures to between 34 C and 36 C have not been associated with a significant increase in
complications such as perioperative bleeding and transfusion requirements.

Decreases in core temperatures to between 34 C and 36 C have not been associated with a significant increase in
postoperative complications such as wound infections.
The general effect of cooling is that all body processes, including neuromuscular function, slow down to the stage
of depression and eventually death.
Moderate degrees of hypothermia are generally indicated for trauma patients.

Regarding the effects of anesthesia and surgery (periopera-tive hypothermia), identify the correct statement.
Induction of general anesthesia results in a gradual decrease in core temperature.
All general anesthetics with the exception of ketamine affect the normal thermoregulatory responses in the same
manner.
Replacement of shed blood with cold or inadequately warmed IV fluids and blood can rarely decrease body
temperature.
Epidural and spinal anesthesia have negligible effects on peripheral and central thermoregulation.

A 64-year-old woman with stable angina is undergoing exploratory laparotomy with general anesthesia following
trauma. Blood loss is 2 L and a fluid warmer was not avail-able. At the end of the 3.5-hour surgery you note

that her core temperature is 34.8 C. Which of the statements is true?
She is not at increased risk of postoperative wound infec-tion.
She is not at increased risk of postoperative ventricular tachycardia and unstable angina.
She is at increased risk of postoperative shivering and prolonged peripheral vasoconstriction.
The most likely cause of her low temperature is monitor-ing error.

7. Intraoperative hypothermia can be safely minimized by:

Maintaining operating room temperature at 19 C

Warming crystalloid solutions to 36 C prior to IV admin-istration and using convective forced-air warming

Warming refrigerated blood products to 36 C in a microwave oven prior to IV administration

Warming crystalloid solutions to 55 C prior to IV admin-istration

ANS WERS

1. a 4. d 6. c
2. a 5. b 7. b
3. d
H YPOTHERMIA IN T R AU M A 461

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