Hyperthermia
Mehrdad Esmailian MD.
Assistant professor of Emergency
Medicine
Definition
► Elevation
of core body temperature above the
normal diurnal range of 36ºC to 37.5ºC due to
failure of thermoregulation
► Hyperthermia is not synonymous with the more
common sign of fever, which is induced by
cytokine activation during inflammation, and
regulated at the level of the hypothalamus
Hyperthermia
► The
most important causes of severe
hyperthermia (greater than 40ºC or 104ºF)
caused by failure of thermoregulation are:
 Heat stroke
 Neuroleptic malignant syndrome
 Malignant hyperthermia
Physiology
► Body
temperature is maintained within a narrow
range by balancing heat load with heat dissipation
► Body's heat load results from both metabolic
processes and absorption of heat from the
environment
► As core temperature rises, the preoptic nucleus of
the anterior hypothalamus stimulates efferent
fibers of the ANS to produce sweating and
cutaneous vasodilation
Physiology
► Evaporation
is the principal mechanism of heat
loss in a hot environment, but this becomes
ineffective above a relative humidity of 75%
► Other methods of heat dissipation
 Radiation- emission of infrared electromagnetic energy
 Conduction- direct transfer of heat to an adjacent,
cooler object
 Convection-direct transfer of heat to convective air
currents
► These
methods cannot efficiently transfer heat
when environmental temperature exceeds skin
temperature
Physiology
► Temperature
elevation  ↑ O2 consumption and
metabolic rate  hyperpnea and tachycardia
► Above 42ºC (108ºF), oxidative phosphorylation
becomes uncoupled, and a variety of enzymes
cease to function
► Hepatocytes, vascular endothelium, and neural
tissue are most sensitive to these effects, but all
organs may be involved
► As a result, these patients are at risk of multiorgan
system failure
Heat Regulation
► The
regulation of body temperature involves
three distinct functions:
 Thermosensors
 Central integrative area
 Thermoregulatory effectors
Thermosensors
► Temperature-sensitive
structures are located
both peripherally in the skin and centrally in
the body
► Skin temperature changes, correlate poorly
with changes in the rate of heat loss
► Thermosensitive neurons are in the preoptic
area of the anterior hypothalamus. They are
activated when the temperature of the blood
circulating through that area exceeds a certain
“set point”
► The
skin temperature affects heat loss, since a
person resting in a warm environment initiates
sweating, even though the core temperature
remains constant
► In contrast, changes in core temperature are
more potent in producing heat-dissipating
responses
Central Integrative Area
► The
CNS interprets information received from
the thermosensors to properly instruct
thermoregulatory effectors
► The concept of a central thermostat by which
an alteration shifts effector thresholds in the
same direction fits a variety of clinical
situations
► For
example, fever, the circadian rhythm of
temperature variation, and the 0.5° C
difference in rectal temperature after ovulation
can be explained by variation of a thermal setpoint
Thermoregulatory Effectors
► Sweating
and peripheral vasodilation are the
major mechanisms by which heat loss can be
accelerated
► In a warm environment, evaporation of sweat
from the skin is the most important mechanism
of heat dissipation
► Heat loss from the skin by convection and
radiation is maximized by increased skin blood
flow to facilitate sweating
► Humans
possess apocrine and eccrine sweat
glands
► Apocrine glands are concentrated in the axillae
and produce milky sweat rich in carbohydrate
and protein. They are adrenergically innervated
and respond to emotional stress as well as to
heat
► Most
glands producing “thermal sweat” are
eccrine glands. These are cholinergically
innervated and distributed over the entire
body, with the largest number on the palms
and soles. Eccrine sweat is colorless, odorless,
and devoid of protein
► Individuals exercising in hot environments
commonly lose 1 to 2 L/hr of sweat; loss of 4
L/hr for short periods is possible
► Cooling
is best achieved by evaporation from
the body surface; sweat that drips from the
skin does not cool the body, and sweat
evaporated from clothing is considerably less
efficient
► Each liter of completely evaporated sweat
consumes 580 kcal of heat
► The
ability of the environment to evaporate
sweat is termed atmospheric cooling power
and varies primarily with humidity, but also
with wind velocity
► As humidity approaches 100%, evaporative
heat loss ceases
► The
vascular response to heat stress is
cutaneous vasodilation and compensatory
vasoconstriction of splanchnic and renal beds
► These vascular changes are under neurogenic
control and allow heat to be dissipated quickly
and efficiently, but they place a tremendous
burden on the heart
► To
maintain blood pressure, cardiac output
must increase dramatically. For this reason,
saunas and hot tubs may be dangerous for
patients with cardiac disease
► Cardiovascular and baroreceptor reflexes also
affect skin blood flow. Reduced forearm
sweating and vasodilation are observed in
severely dehydrated subjects exercising in a
warm environment
Acclimatization
► Definition
: constellation of physiologic
adaptations that appear in a normal person as
the result of repeated exposures to heat stress
► Daily exposure to work and heat for 100
min/day results in near-maximal acclimatization
in 7 to 14 days. This is characterized by an
earlier onset of sweating (at a lower core
temperature), increased sweat volume, and
lowered sweat electrolyte concentration
► Acclimatization
is hastened by modest salt
deprivation and delayed by high dietary salt
intake
► As acclimatization proceeds, the sweat sodium
concentration drops while the volume increases
► The
cardiovascular system plays a major role in
both acclimatization and endurance training,
largely resulting from an expansion of plasma
volume
► Heart rate is lower and associated with a
higher stroke volume
► Other
physiologic changes include :
► Earlier
release of aldosterone, although
acclimatized individuals generate lower plasma
levels of aldosterone during exercise heat
stress
► Total body potassium depletion of up to 20%
(500 mEq) by the second week of
acclimatization can occur as a result of sweat
and urine losses coupled with inadequate
repletion
► The
well-conditioned athlete is not necessarily
heat acclimatized
► To
maintain heat and exercise-induced
adaptive responses, heat exposure needs to
continue intermittently at least on 4-day
intervals
► Plasma volume decreases considerably within 1
week in the absence of heat stress
Predisposing Factors
► Elderly
patients or those with chronic diseases
who are taking medications predisposing to
heat illness are prone to classic heatstroke
during periods of high ambient heat and
humidity. Adequate fluid intake is essential.
► Elderly
patients
sometimes
dress
inappropriately for hot weather; heat loss is
maximized by light, loose-fitting garments
► Exertional
heatstroke is most likely to occur in
young, healthy people involved in strenuous
physical activity, especially if they have not
acclimatized
► Fluid intake is the most critical variable.
Dehydration can be minimized by education on
work-rest cycles and fluid consumption and
through provision of cool, pleasantly flavored
fluids
► The
goal is to maximize voluntary fluid intake
and gastric emptying so that fluid can rapidly
enter the small intestine, where it is absorbed
► Gastric emptying is accelerated to 25 mL/min
by large fluid volumes (500-600 mL) and cool
temperatures (10° C to 15.8° C)
► High osmolality inhibits gastric emptying;
osmolality of less than 200 mOsm/L is optimal
► Hydration
can be monitored by measuring
body weight before and after training or
athletic competition
► An athlete with a loss of 2% to 3% body
weight (1.5-2 L in a 70-kg man) should
drink extra fluid and be permitted to
compete only when within 0.5 to 1 kg (1-2
pounds) of the starting weight on the
previous day
►A
weight loss of 5% to 6% represents a
moderately severe deficit and usually is
associated with intense thirst, scanty urine,
tachycardia, and an increase in rectal
temperature of about 2° C. Such athletes
should be restricted to light workouts after
hydration to their normal weight
►A
loss of 7% or more of body weight
represents severe water depletion; the athlete
should not participate in sports until examined
by a physician. Wrestlers frequently fast,
restrict food and fluid intake, and exercise
vigorously wearing vapor-impermeable clothing
to lose weight quickly so that they can
compete in a lower weight class
► The
administration of salt tablets during
strenuous exercise can cause delayed gastric
emptying, osmotic fluid shifts into the gut,
gastric mucosal damage, and hypernatremic
dehydration
► A 6-g sodium diet is sufficient for successful
adaptation for work in the heat, with sweat
losses averaging 7 L/day
► Excessively
high salt intake in relation to salt
losses in sweat during initial heat exposure can
impair acclimatization because of inhibition of
aldosterone secretion
► Excessive salt ingestion can also exacerbate
potassium depletion
► Evaporative
cooling can be lost when clothing
inhibits air convection and evaporation
► Loose-fitting clothing or ventilated fishnet
jerseys allow efficient evaporation
► Light-colored clothing reflects rather than
absorbs light
► Water evaporated from clothing is much less
efficient for body cooling than is water
evaporated from the skin
► The
body's heat dissipation mechanisms are
analogous to the cooling system of an
automobile : Coolant (blood) is circulated by a
pump (heart) from the hot inner core to a
radiator (skin surface cooled by the
evaporation of sweat). Temperature is sensed
by a thermostat (CNS), which alters coolant
flow by a system of pipes, valves, and
reservoirs (vasculature)
MINOR HEAT ILLNESS
► Heat
Cramps
► Heat Edema
► Heat Syncope
► Prickly Heat
MAJOR HEAT ILLNESS
► HEAT
EXHAUSTION
► HEATSTROKE
 Classic
 Exertional
Heat Cramps
► Brief,
intermittent, and often severe muscular
cramps occurring typically in muscles that are
fatigued by heavy work
► Heat cramps occur most commonly during the
first days of work in a hot environment and
develop in persons who produce large amounts
of thermal sweat and subsequently drink
copious amounts of hypotonic fluid
► Heat cramps appear to be related to salt
deficiency
► The
most commonly victims : athletes, roofers,
steel workers, coal miners, field workers, and
boiler operators
► Heat cramps tend to occur after exercise when
the victim has stopped working and is relaxing.
In this respect, they differ from the cramps
experienced by athletes during exercise, which
tend to last for several minutes, are relieved by
massage, and resolve spontaneously
► Essentials
of Diagnosis :
 Cramps of most worked muscles
 Usually occur after exertion
 Copious sweating during exertion
 Copious hypotonic fluid replacement during
exertion
 Hyperventilation not present in cool
environment
► DDs
: hyperventilation tetany
► Heat cramp victims exhibit hyponatremia,
hypochloremia, and low serum sodium and
chloride levels
► Rhabdomyolysis or resultant renal damage is
not present with isolated heat cramps
Management
► Mild
cases without concurrent dehydration may
be treated orally with 0.1% to 0.2% salt
solution (two to four 10-grain salt tablets [56
to 112 mEq] or ¼ to ½ teaspoon table salt
dissolved in a quart of water), which is the
general limit of palatability
► Severe cases respond rapidly to intravenous
isotonic solution (0.9% NaCl)
► Salt tablets are gastric irritants and are not
recommended
Heat Edema
► Swollen
feet and ankles are often reported by
nonacclimatized individuals, especially the
elderly, who encounter climatic stresses of
tropical and semitropical area
► Such individuals often have no underlying
cardiac, hepatic, venous, or lymphatic disease.
They commonly have assumed rigorous
schedules with long periods of sitting or
standing
►
The edema is usually minimal, not
accompanied by any significant impairment in
function, and often resolves after several days
of acclimatization
► It
is presumed that hydrostatic pressure and
vasodilation of cutaneous vessels, combined
with some degree of orthostatic pooling, lead
to vascular leak and accumulation of interstitial
fluid in the lower extremities
► Aldosterone increases in response to the heat
stress and perceived central volume deficit
► Awareness
of this clinical presentation prevents
overly vigorous diagnostic and therapeutic
intervention
► Brief
diagnostic evaluation to rule out
thrombophlebitis, lymphedema, or congestive
heart failure is appropriate, but invasive
diagnostic
techniques
or
vigorous
pharmacologic therapy is not indicated
Management
► No
evidence exists that diuretic therapy is
effective
► Leg elevation or thigh-high support hose
► In most individuals, the problem resolves either
through adequate acclimatization or with the
individual's return to a home climate
Heat Syncope
► The
elderly have a special predilection for this
disorder
► Individuals adapt to a hot, humid environment
by dilation of cutaneous vessels to deliver heat
to the body surface. Thus, an increased portion
of the intravascular pool is located in the
periphery at any given time
► Increasing
blood flow to compliant cutaneous
veins raises skin vascular volume at the
expense of thoracic blood volume. Individuals
who stand for protracted periods tend to pool
blood in the lower extremities
► Combined with volume loss and peripheral
vasodilation, this pooling can result in
inadequate
central
venous
return,
a
concomitant drop in cardiac output, and a
cerebral perfusion inadequate to maintain
consciousness
Management
► The
disorder
is
self-limited,
because
assumption of a horizontal position is the cure
► Individuals at risk for heat syncope should be
warned to move often, flex leg muscles
repeatedly when standing stationary, avoid
protracted standing in hot environments, and
assume a sitting or horizontal position when
prodromal warning signs or symptoms occur
► prodromal
warning signs or symptoms :
 scintillating scotomata
 tunnel vision
 Vertigo
 Nausea
 Diaphoresis
 weakness
 Adequate education prevents many serious
injuries
Prickly Heat
► Prickly
heat, also known as miliaria rubra,
lichen tropicus, and heat rash, is an acute
inflammatory disorder of the skin that occurs in
tropical climates
► It is the result of blockage of sweat gland
pores by macerated stratum corneum and
secondary staphylococcal infection
► The
acute phase is characterized by vesicles in
the malpighian layer of the skin caused by
dilation and rupture of the obstructed sweat
gland ducts
► Clinically, this initially produces intensely
pruritic vesicles on an erythematous base. The
rash is confined to clothed areas, and the
affected area is often completely anhidrotic
► Over
the next week or so, a keratin plug arises
and fills these vesicles, causing a deeper
obstruction of the sweat gland duct. The
obstructed duct then ruptures a second time,
producing a deeper vesicle within the dermis.
This is known as the profunda stage, and it can
persist for weeks. Profunda vesicles are not
pruritic and closely resemble the white papules
of piloerection
► Chronic dermatitis is a common complication
Management
► Chlorhexidine
in a light cream or lotion is the
antibacterial treatment of choice during the
acute phase
► Salicylic acid, 1%, can be applied three times
daily to localized, affected areas to assist in
desquamation, but it should not be used over
large areas because of possible salicylate
intoxication
► For diffuse or pustular rashes, erythromycin
can be helpful
► Prickly
heat can be prevented by wearing light,
loose-fitting, clean clothing and avoiding
situations that produce continuous sweating
► Routine use of talcum or baby powder should
be avoided
► Spending 8 to 12 hours a day in an airconditioned environment is helpful
Heat Exhaustion
► Volume
depletion that occurs under conditions
of heat stress
► Types: water depletion / salt depletion
► Water depletion heat exhaustion results from
inadequate fluid replacement by individuals
working in a hot environment
► This
“voluntary dehydration” results in
progressive hypovolemia
► Salt
depletion heat exhaustion takes longer to
develop than the water depletion form. It
occurs when large volumes of thermal sweat
are replaced by water with too little salt
► It differs from heat cramps in that systemic
symptoms occur
► This
syndrome
is
characterized
by
hyponatremia, hypochloremia, and low urinary
sodium and chloride concentrations
► Body temperature usually remains near normal
Clinical Features
Weakness
 Fatigue
 frontal headache
 impaired judgment
 Vertigo
 nausea and vomiting
 muscle cramps
 Orthostatic dizziness and syncope

► The
core temperature is only moderately
elevated, usually less than 40° C, and signs of
severe CNS dysfunction are not present
Diagnosis
► Vague
malaise, fatigue, headache
► Core temperature often normal; if elevated,
less than 40° C (104° F)
► Mental function essentially intact; no coma or
seizures
► Tachycardia, orthostatic hypotension, clinical
dehydration (may occur)
► Other major illness ruled out
► If in doubt, treat as heat stroke
► Elevations
of hepatic transaminases to several
thousand units can be seen in patients with
heat exhaustion or healthy runners after a
marathon, whereas in patients with heatstroke,
such levels are usually in the tens of thousands
after 24 hours
Management
► Heat
exhaustion is primarily a volume depletion
problem, and rapid recovery generally follows
fluid administration
► Decisions regarding the type of fluid and
electrolyte replacements should be based on
serum electrolyte measurements and the
estimation of hydration status by clinical and
laboratory parameters
► In
mild cases, rest in a cool environment and
an oral electrolyte solution, such as 0.1%
saline, may suffice
► Patients with significant volume depletion or
electrolyte abnormalities generally require
intravenous fluids
► If the patient is orthostatic, normal saline
should be administered until the patient is
hemodynamically stable
► Free
water deficits should be replaced slowly
over 48 hours so as not to decrease serum
osmolality more than 2 mOsm/hr
► Overly rapid correction of hypernatremia is
associated with seizures caused by cerebral
edema
Disposition
► Young,
otherwise healthy patients who do not
have significant laboratory abnormalities and
who respond rapidly to treatment do not
require hospitalization. These patients can be
discharged with instructions to drink plenty of
fluids and avoid heat stress for 24 to 48 hours.
► Older
patients, particularly those with
cardiovascular disease or other predisposing
factors, require more cautious fluid and
electrolyte
replacement
and
frequent
reassessment
► Admission if patient is elderly, has significant
electrolyte abnormalities, or would be at risk
for recurrence if discharged
Treatment




Rest
Cool environment
Assess volume status (orthostatic changes,
BUN, hematocrit, serum sodium)
Fluid replacement: normal saline to replete
volume if patient orthostatic, replace free water
deficits slowly to avoid cerebral edema
Heat Stroke
► Body
temperature rises with fails in
homeostatic thermoregulatory mechanisms
► This failure results in elevation of body
temperature to extreme levels, usually greater
than 40.5° C (105° F), producing multisystem
tissue damage and organ dysfunction
► Core
body temperature > 40.5ºC (105ºF) with
associated CNS dysfunction in the setting of a
large environmental heat load that cannot be
dissipated
► Complications include:
 ARDS
 DIC
 Renal or hepatic failure
 Hypoglycemia
 Rhabdomyolysis
 Seizures
► The
resultant damage to tissues depend on :
 Body temperature
 Exposure time
 Work load
 Tissue perfusion
 Individual factors
► Neurologic
dysfunction is a hallmark of
heatstroke, and cerebral edema is common
► Other pathologic changes include :
 petechiae in the walls of the third and fourth
ventricles
 marked cerebellar Purkinje cell damage
 The hypothalamus, the predominant site of
central thermoregulatory control, is usually not
damaged
► Heat
stress creates tremendous demands on
the cardiovascular system, and signs of
circulatory failure, increases in skin blood flow
(peripheral vasodilation) and a reduction of the
thermal gradient between the core and the
skin
► Compensatory
vasoconstriction
of
the
splanchnic and renal vasculature. The resulting
splanchnic and renal ischemia may explain the
nausea, vomiting, and diarrhea observed in
postmarathon runners
► Hepatic damage : centrilobular necrosis with
extensive cholestasis
► Failure
to perfuse the skin with heated blood
from the core results in a dramatically
increased rate of heat storage. This produces
RICP, which, in combination with a reduction in
MAP caused by failure of compensatory
splanchnic vasoconstriction, conspires to
produce a fall in cerebral blood flow; this
results in the major CNS dysfunction
characteristic of heatstroke
Diagnosis





Exposure to heat stress, endogenous or
exogenous
Signs of severe CNS dysfunction
(coma,seizures, delirium)
Core temperature usually above 40.5° C (105°
F), but may be lower
Dry, hot skin common, but sweating may
persist
Marked elevation of hepatic transaminases
Classic (nonexertional) heat stroke
► Affects
individuals with underlying chronic medical
conditions that either impair thermoregulation or
prevent removal from a hot environment.
► Conditions include:






Cardiovascular disease
Neurologic or psychiatric disorders
Obesity
Anhidrosis
Extremes of age
Anticholinergic agents or diuretics
► Occurs
during periods of sustained high
ambient temperatures and humidity, as during
summer heat waves
► Victims are often elderly and poor and live in
underventilated
dwellings
without
air
conditioning
► Debilitated patients who have limited access to
oral fluids may develop water-depletion heat
exhaustion, which progresses to heatstroke if
untreated
► Victims
of CHS commonly suffer from chronic
diseases, alcoholism, or schizophrenia, which
predispose to heat illness. Such patients are
often prescribed medications (e.g., diuretics,
antihypertensives,
neuroleptics,
and
anticholinergics) that impair the ability to
tolerate heat stress
► Sweating is totally absent in the majority of
CHS patients
► Poor
outcome critria :
 Advanced age
 Hypotension
 Altered coagulation status
 The necessity for endotracheal intubation on
arrival at the emergency department
Exertional heat stroke
► Occurs
in young, otherwise healthy individuals
engaged in heavy exercise during periods of
high ambient temperature and humidity
► Findings include : cutaneous vasodilation,
tachypnea, rales due to noncardiogenic
pulmonary edema, excessive bleeding due to
DIC, altered mentation or seizures
► Labs: coagulopathy, ARF, elevated LFTs due to
acute hepatic necrosis, respiratory alkalosis,
and a leukocytosis as high as 30,000 to
40,000/mm3
► Rhabdomyolysis
and ARF, rarely seen in
patients with CHS, are common in patients
with EHS
► Sweating is present in half the cases of EHS
► Hypoglycemia
► Coagulopathy
► Hyponatremia with serum sodium levels less
than 130 mmol/L (neurologic symptoms or
seizures)
► Delirium
or coma is characteristic, but virtually
any neurologic abnormality, including bizarre
behavior,
opisthotonus,
hallucinations,
decerebrate rigidity, oculogyric crisis, and
cerebellar dysfunction, can be seen
► Convulsions occur in up to 75% of patients and
can be precipitated by therapeutic maneuvers
(such as ice water immersion)
► Profound
muscle
rigidity
with
tonic
contractions, coarse tremor, and dystonic
movements can mimic seizures
► Pupils may be fixed and dilated, and the
electroencephalogram may be isoelectric
► All these changes are potentially reversible,
although
permanent
damage,
including
cerebellar deficits, hemiplegia, dementia, and
personality changes, is common in severe
cases
► Patients
with heatstroke usually have
hyperdynamic cardiovascular systems with low
peripheral vascular resistance, tachycardia (up
to 180 beats/min), and an elevated cardiac
index. These changes are expected because
skin blood vessels dilate to dissipate heat;
however, this low peripheral vascular
resistance has persisted in patients treated
with ice water immersion and reduction of
body temperature to near normal
► CVP
is usually elevated
► The combination of elevated CVP with rightsided cardiac dilation suggests right-sided
cardiac failure, which is also seen after shock
or sepsis
► Respiratory alkalosis is a physiologic response
to active or passive heating and may be severe
enough to produce tetany
► Although
most patients with CHS have
respiratory alkalosis, those with EHS usually
have a relatively pure lactic acidosis
► Lactic acidosis is associated with a poor
prognosis in cases of CHS but not necessarily
in cases of EHS
► Aberrations
in coagulation are common in
patients with severe heatstroke, and their
presence is a poor prognostic sign
► Abnormal hemostasis is manifested clinically by
purpura, conjunctival hemorrhage, melena,
bloody diarrhea, hemoptysis, hematuria,
myocardial bleeding, or hemorrhage into the
CNS
► Hepatic
injury is evidenced by markedly
elevated levels of hepatic aminotransferases
(serum aspartate transaminase and alanine
transaminase)
► Jaundice typically appears 24 to 72 hours after
the onset of severe heatstroke and gradually
recedes if the victim survives
► Survivors
generally have no permanent
impairment of liver function
► Hypoglycemia
with a serum glucose level less
than 65 mg/dL is common in cases of
exertional heatstroke
► Renal damage is common. The initial urine
specimen, usually obtained by catheterization,
is a scanty, brownish, turbid fluid resembling
machine oil
► Microscopic
examination reveals proteinuria
with abundant granular casts and red blood
cells
► Acute oliguric renal failure complicates 25% to
30% of EHS cases and 5% of CHS cases
► Glomerular filtration rate, renal plasma flow,
urine flow, and sodium excretion diminish
markedly during exercise
► Heavy
physical exertion in hot climates
produces acidic and maximally concentrated
urine, which can result in acute oliguric renal
failure when combined with hypotension and
myoglobinuria
► Cocaine
use is also associated with
rhabdomyolysis and hyperthermia
► Diarrhea,
probably caused by intense
splanchnic vasoconstriction, is commonly seen
► Cooling aggravates the diarrhea, creating an
unpleasant treatment problem
► Pancreatitis is described with elevated serum
amylase and lipase levels
Diagnosis
► Thermometry


:
Oral thermometry is affected by mouth
breathing and is a poor approximation of the
core
Rectal thermometry is less variable but
responds to changes in core temperature
slowly



Thermistors that are inserted 15 cm into the
rectum offer continuous monitoring of
temperature and less variability
Although slower to respond to changes in core
temperature than tympanic temperature
readings, rectal measurements are not biased
by head skin temperature
An esophageal thermistor positioned adjacent
to the heart is another option



Placement of a tympanic temperature sensor
directly on the tympanic membrane may be
difficult and is not used clinically
Commercially available infrared thermometers
do not physically contact the tympanic
membrane and are unreliable in detecting
hyperthermia
If a patient is being monitored with a catheter,
pulmonary arterial temperature can be
measured precisely with a thermistor catheter
Management
► Ensure
ABCs,
complications
initiate
rapid
cooling,
tx
Management
Cooling
► Immediate
cooling
is
the
cornerstone of
treatment
► Cooling must be initiated as soon as possible,
in conjunction with the initiation of stabilizing
treatment
► Mortality increases significantly when cooling is
delayed
► In
the prehospital setting, cooling should be
initiated by removing the patient from the hot
environment and fanning
► When the patient arrives at the hospital,
clothes should be removed, a thermistor probe
should be inserted, and the temperature
should be continuously monitored
► The
ideal method of evaporative cooling uses a
body cooling unit on which the patient lies
suspended on a net surface while being
sprayed with atomized 15° C water from above
and below
► Air warmed to 45° C to 48° C is blown over the
skin surface at 3 m/min. The unit, not widely
available, maximizes evaporative cooling by
maintaining
cutaneous
vasodilation
and
avoiding heat generation caused by shivering
► Evaporative
cooling is the most widely used
cooling method
► The combination of atomized tepid water at
40° C from a spray bottle and standing fans
cool at rates comparable to both body cooling
unit and immersion
► Other evaporative techniques, including the
use of downdraft from a helicopter
► Immersion
in ice water results in a rapid
reduction of core temperature to less than
39° C within 10 to 40 minutes
► When the body temperature reaches 39° C,
cooling measures should be discontinued to
avoid hypothermic overshoot
► Continuous monitoring is necessary to maintain
the core temperature at 37° C to 38° C
► Cooling
modalities other than evaporation and
immersion should be considered adjunctive
treatments
► Application of ice packs to high heat transfer
areas (neck, groin, axillae) is commonly used
► Cooling blankets may be a useful adjunct but
will not produce rapid cooling if used
exclusively
► Cardiopulmonary
bypass with a heat exchanger
has been successful in the treatment of
malignant hyperthermia
► Peritoneal dialysis with cold fluids, although
successful in a canine model, remains untested
in humans
► Cold-irrigant gastric or rectal lavage will not
provide significant heat exchange if used as
the primary cooling modality
Resuscitation
► Aspiration
and seizures are common in patients
with heatstroke, and airway control is essential
► Hypoxemia may occur because of aspiration,
pneumonitis
and
pulmonary
infarction,
hemorrhage, or edema
► Metabolic demands are high, and normal
pulmonary ventilation may be inadequate in
this setting
► Circulatory
fluid requirements are modest in
some cases, averaging 1200 mL of isotonic
crystalloid solution in the first 4 hours
► Pulmonary edema occurs in patients with
heatstroke and can be exacerbated by
overzealous fluid administration
► The use of a CVP catheter to monitor fluid
resuscitation may be deceptive
► Most
patients have a hyperdynamic circulation
with high cardiac index, low peripheral vascular
resistance, and elevated CVP as a result of
right-sided heart failure. These patients may
require only modest intravenous fluids because
cooling
produces
vasoconstriction
and
increases blood pressure
► Hypotension
is common in patients with
heatstroke and is usually caused by peripheral
vasodilation resulting in high-output cardiac
failure, in addition to dehydration
► Blood pressure usually rises with cooling
► If
the patient has a low central venous or
pulmonary capillary wedge pressure, a fluid
challenge of 250 to 500 mL of 0.9% saline
should be given rapidly while blood pressure,
pulse, and urine output are monitored
► If the blood pressure rises, further fluids are
given with careful monitoring of the CVP.
Aggressive fluid replacement is continued until
the blood pressure reaches 90/60 mm Hg or
the CVP exceeds 12 mL H2O
► Occasionally,
patients exhibit hypodynamic
responses with low cardiac index, elevated
CVP, and hypotension. These patients may be
cyanotic, whereas patients with hyperdynamic
circulation are initially pink
► This clinical observation can be helpful in
identifying patients who may respond to
catecholamines
►A
variety of tachyarrhythmias commonly occur
during heatstroke. These usually resolve with
cooling, and electrical cardioversion should be
avoided until the myocardium is cooled
► The use of p -adrenergic agents such as
norepinephrine is not recommended because
they
promote
vasoconstriction
without
improving cardiac output or perfusion,
decrease cutaneous heat exchange, and may
enhance ischemic renal and hepatic damage
► Atropine
and other anticholinergic drugs that
inhibit sweating should be avoided
► Antipyretics such as aspirin and acetaminophen
are not indicated and may be harmful
► Salicylates, particularly in large doses, can
worsen hyperthermia by uncoupling oxidative
phosphorylation and aggravate coagulopathies
► Large
doses of acetaminophen can result in
further hepatic damage
► The efficacy of dantrolene is not established
► After
volume repletion, administration of
mannitol in an initial intravenous dose of 12.5
g, followed by 12.5 g mannitol per liter of
intravenous fluid increases renal blood flow
and minimizes damage from myoglobinuria
secondary to rhabdomyolysis
► If myoglobinuria is documented, maintenance
of urine output of at least 50 mL/hr and urinary
alkalinization are indicated
► Dextran
is contraindicated because of its
propensity to coat platelets and impair
coagulation
► Persistent anuria, uremia, or hyperkalemia is
an indication for consideration of hemodialysis
► Hematologic evaluation
 ABG
 CBC and platelet counts
 Electrolytes
 BUN/Cr
 Glucose
 AST/ALT
 LDH, CPK
 Cric and lactic acid
 Calcium levels
 PT/PTT/INR
 FDP
:
► Acidosis
is common, especially in patients with
exertional heatstroke
► Lactate levels are usually elevated; this may
persist or even worsen with improved
extremity perfusion
► Cooling
modalities that drastically lower skin
temperature may induce violent shivering; this
increases metabolic heat production and may
impede cooling
► In this situation, chlorpromazine (25 mg IV)
can be efficacious. Chlorpromazine has
anticholinergic properties that can interfere
with sweating and cause hypotension or,
rarely, precipitate seizures
► Many
patients are agitated during the initial
cooling period. Short-acting benzodiazepines
can be used for sedation and to control
seizures
► Barbiturates are less desirable for treatment of
seizures, since metabolism is altered by hepatic
dysfunction
► Coagulopathies
can occur during the first day
of illness but are more common on the second
and third days. Initial treatment should include
replacement therapy with FFP and platelets
► The clinician should monitor the laboratory
signs of DIC (hypofibrinogenemia, elevated
fibrin split products, prolonged prothrombin
time, and thrombocytopenia)
► The
bleeding diathesis in patients with
heatstroke may be the result of fibrinolysis.
Although amino caproic acid can impede
fibrinolysis, administration of this compound is
associated with rhabdomyolysis and its use is
not recommended in patients with heatstroke
DDs
► When
a history of collapse under conditions of
heat stress is present, rapid improvement in
mental status and blood pressure with cooling
eliminates alternative diagnoses
► If the temperature does not respond and the
patient does not recover neurologically, other
causes of fever and coma must be considered



Shaking chills suggest fever with an altered
hypothalamic set point rather than heat illness
(Meningitis and encephalitis)
In patients with heatstroke, the spinal fluid
should be crystal clear, with occasional
lymphocytic pleocytosis and elevated protein
levels
Cerebral falciparum malaria, which presents a
clinical picture of high fever and encephalitis, is
seen in tropical areas




In patients with thyroid storm, the clinical
symptoms resemble those of heatstroke
It should be suspected if the thyroid gland is
enlarged or nodular, but a normal thyroid
gland does not exclude the diagnosis
Thyroid function test results are elevated, but
these are not available on an emergency basis
Thyroid storm is rare, and some critical aspects
of treatment, such as rapid cooling, coincide
with those for heatstroke


Drug-induced heat illness is an important
consideration,
particularly
anticholinergic
poisoning
Differentiation may be difficult because both
heatstroke and anticholinergic poisoning
produce hyperpyrexia, hot and dry skin,
tachycardia, and abnormal mental status



Constricted pupils are present in many
heatstroke patients
Mydriasis should be present in patients with
anticholinergic poisoning, and its absence
argues strongly against this diagnosis
Typhoid fever, typhus, delirium tremens, and
hypothalamic hemorrhage
Malignant Hyperthermia
► Rare
genetic disorder manifests after
administration
of
anesthetic
agents:
succinylcholine and halothane
► Onset is usually in 1 hour of the administration
of anesthesia, rarely delayed up to 10 hours
► ½ of cases are inherited in as AD; Rest are
inherited in different patterns
► Early
clinical
findings
in
malignant
hyperthermia include : muscle rigidity
(especially
masseter
stiffness),
sinus
tachycardia, increased CO2 production, and
skin cyanosis with mottling
► Marked hyperthermia (up to 45ºC [113ºF])
occurs minutes to hours later; core body
temperature tends to rise 1ºC every 5 to 60
minutes
Malignant Hyperthermia
► Hypotension,
complex
dysrhythmias,
rhabdomyolysis, electrolyte abnormalities, DIC
and mixed acidosis accompany the elevated
temperatur
► Rarely,
biochemically-proven
malignant
hyperthermia may present solely with
rhabdomyolysis in the absence of hyperthermia
Neuroleptic malignant syndrome
► Idiosyncratic
reaction to antipsychotic agents
► IN addition to hyperthermia, NMS is also
characterized by "lead pipe" muscle rigidity,
altered
mental
status,
choreoathetosis,
tremors,
and
evidence
of
autonomic
dysfunction, such as diaphoresis, labile blood
pressure, and dysrhythmias
Diagnostic Evaluation
► Get
a rectal temperature; abnormal VS include
sinus tachycardia, tachypnea, widened pulse
pressure, hypotension
► CXR may demonstrate pulmonary edema
► ECG may reveal dysrhythmias, conduction
disturbances, nonspecific ST-T wave changes, or
heat-related myocardial ischemia or infarction
► Labs:
CBC CCP, Coagulation Studies, creatine
kinase, and check for hyperphosphatemia,
myoglobinuria
► Myoglobinuria should be suspected in a patient
who has a brown urine supernatant that is
heme-positive, and clear plasma.
► Toxicologic screening may be indicated if a
medication effect is suspected.
► Head CT and lumbar puncture if CNS etiologies
suspected
► Diagnosis
confirmed by in vitro muscle
contracture test following recovery from the
acute hyperthermic episode
► Abnormal augmentation of in vitro muscle
contraction following treatment with halothane
or caffeine is diagnostic of the disorder
► However,
this test is expensive, not widely
available, and frequently not covered by
insurance
► Genetic testing for the more than 40 known
mutations of the SKM ryanodine receptor
(RyR1) can be used in conjunction with the in
vitro muscle contracture test to evaluate
individual susceptibility in patients from
families with a history of malignant
hyperthermia
Malignant hyperthermia
Management:
► Dantrolene
administration is the mainstay of
treatment of malignant hyperthermia, and
should be initiated as soon as the possible
► With dantrolene administration, the mortality of
the fulminant syndrome has fallen from %70
to less than %10
► Dantrolene is a nonspecific SKM relaxant that
acts by blocking the release of calcium from
the SR  decreases the myoplasmic
concentration of free calcium and diminishes
the myocyte hypermetabolism that causes
clinical symptoms
►A
2 mg/kg IV bolus is given and should be
repeated every 5 minutes until symptoms
abate up to a maximum dose of 10 mg/kg
► This may be repeated every 10 to 15 hours.
After an initial response, the drug should be
continued orally at a dose of 4 to 8 mg/kg per
day, in four divided doses, for three days