Heat Stroke and Heat Exhaustion

Sholihul Muhibbi

Fever vs Hyperthermia

Fever
Elevation of body temperature above the normal range as the
result of a change in the thermoregulatory center located in
the anterior hypothalamus.
The elevation of the bodys normal set point occurs through
the release of pyrogenic cytokines including: IL-1, TNF, IFNgamma, IL-6 and their effects in the hypothalamus.
Elevation in temperature results from either increased heat
production (shivering) or decreased loss (peripheral
vasoconstriction).

Fever vs Hyperthermia
Hyperthermia

Elevation of body temperature above the

hypothalamic set point due to insufficient heat
dissipation
The bodys metabolic heat production or
environmental heat load exceeds the bodys ability to
lose heat or energy
Not mediated by cytokines

Hyperthermia Differential
Heat Stroke
Drug-induced hyperthermia
Neuroleptic malignant syndrome
Malignant hyperthermia
Endocrinopathy

Drug-induced hyperthermia

Sympathomimetic poisoning
cocaine, methamphetamines, and amphetamines
Effects produced by raising synaptic concentrations of NE,
Dopamine, and serotonin

Anticholinergic poisoning syndrome

Antihistamines, atropine, diphenhydramine, etc
Effects result from blockade of muscarinic acetylcholine
receptors
Physostigmine raises acetylcholine concentrations

Neuroleptic Malignant Syndrome

Definition-Idiosyncratic reaction to certain medications
characterized by muscle rigidity, hyperthermia, autonomic
instability, and altered mental status
Cause- appears to be caused by the inhibition of central
dopamine receptors in the hypothalamus, which increases heat
generation and decreased heat loss
Drugs

Phenothiazines, haloperidol, thiothixene, TCA, MAO

Treatment- Early recognition of NMS, immediate

discontinuation of suspected medications, supportive care,
increasing dopaminergic activity (bromocroptine)

Malignant hyperthermia
Definition- Rare clinical syndrome characterized by hyperthermia,
muscle rigidity, and metabolic acidosis seen in individuals undergoing
general anesthesia.
Pathophysiology- inherited abnormality of skeletal muscle SR that
causes rapid increase in intracellular calcium levels in response to
certain drugs.
Drugs

General anesthetics- halothane, enflurane, isoflurane

Muscle relaxants- succinylcholine

Treatment
Dantrolene- a direct skeletal muscle relaxant
Procainamide remains the DOC for cardiac dysrhythmias

Endocrinopathy
Thyrotoxicosis
Pheochromocytoma

Conductive heat loss

Conduction- the direct transfer of heat from skin

to the surrounding air also occurs, but with

diminished efficiency as the ambient temp rises.

Radiant heat loss

Radiation- passive transfer of heat from a

warmer to cooler object.

Accounts for 65% of body heat loss under
normal conditions.
Radiant heat losses decrease as temperature of
the surrounding environment increases up to
99.0 F at which point heat transfer reverses
direction.

Heat dissipation
Sweat production and evaporation are the major

mechanisms of heat removal.

At normal temps evaporation accounts for ~20%
of the bodys heat loss, but becomes the major
mechanism for heat loss at higher temps.
Sweat loss can be as much as 2.5 L/h with
vigorous exertion at elevated temps.
Limited as humidity increases.

Impairment of heat loss

General health conditions-

obesity, generalized skin diseases, diminished

cutaneous blood flow, dehydration, malnutrition,
hypotension, reduced cardiac output.
Medications

Impair sweating- Anticholinergics, antihistamines,

TCA, MAO, diuretics
Reduce cutaneous blood flow- vasoconstrictors, Badrenergic blocking agents

Heat induced illness

Heat syncope
Heat cramps
Heat exhaustion
Heat stroke

Heat syncope
Loss of consciousness can result from

cutaneous vasodilation with consequent

systemic and cerebral hypotension
Typically a history of vigorous physical activity
prior to syncopal episode
Skin is typically cool and moist, with weak pulse
Tx includes rest, cooler environment, oral fluids

Heat cramps
Slow painful muscle contractions cramps

resulting from fluid and electrolyte depletion

Typically involves muscles most heavily used
Cramping results from salt depletion as sweat
losses are replaced with water alone
Temperature usually normal
Oral fluid hydration

Heat exhaustion

Definition-heat illness characterized by volume

depletion that occurs under conditions of heat stress.
Water depletion- results from inadequate fluid replacement
by individuals working in a hot environment (laborers,
athletes, military personel)
Salt depletion - large volumes of thermal sweat are replaced
by water with too little salt. Differs from heat cramps in that
systemic symptoms occur. Often with hyponatremia,
hypochloremia, and low urinary sodium.

Heat exhaustion: diagnosis

Vague malaise, fatigue, headache, N/V, cramps
Increased pulse, skin usually moist
Core temperature only mildly elevated, usually

less than (104F)

Tachycardia, orthostatic hypotension
Mental function essentially intact, no signs of
severe CNS damage (e.g., no coma or seizures)

Heat exhaustion: treatment

Rest
Cool environment
Assess volume status (orthostatic changes, BUN,
hematocrit, serum sodium)
Fluid replacement:

oral hydration is prefered in pts who are conscious, coherent,

and without N/V or diarrhea.
NS to replete volume if orthostatic, replace free water deficits
slowly to avoid cerebral edema

Heat stroke
Life threatening medical emergency resulting

from failure of the bodys normal

thermoregulatory mechanisms resulting in
elevation of body temperature to extreme levels
usually greater the (106F) producing
multisystem tissue damage and organ
dysfunction.

Pathophysiology
Specific cellular mechanism underlying the failure of
thermoregulatory homeostatis is not completely
understood.
Damage is a function of both temperature and exposure
time.
circulating concentrations of ICAM1, endothelin, and
von Willebrand factor-antigen are significantly increased
in heat stroke patients suggesting endothelial
activation/injury.

Pathophysiology
Prolonged heat stress produces significant increases in
peripheral vasodilation as skin blood vessels dilate in an
attempt to dissipate heat eventually producing a
reduction of the thermal gradient between the core and
the skin.
As severe heat stress continues, the cutaneous blood
flow decreases and failure to perfuse the skin with
heated blood from the core results in dramatically
increased rate of heat storage.

pathophysiology
Functional hypovolemia is avoided by compensatory
vasoconstriction of the splanchnic and renal vasculature
which may explain the nausea, vomiting, and diarrhea.
Cerebral edema and cerebrovascular congestion that
occur with hyperthermia produce elevated intracranial
pressure, which coupled with a reduction in mean
arterial pressure caused by failure of compensatory
splanchnic vasoconstriction, produces a fall in cerebral
blood flow resulting in the major CNS dysfunction seen
in heat stroke.

Exertional heat stroke

Typically occurs in younger individuals involved

in strenuous activity at high ambient

temperatures and/or humidity. (Athletes and
military recruits)
otherwise healthy people whose heat dispelling
mechanisms are overwhelmed by endogenous
heat production.

Classic heat stroke

Victims are usually aged, often bedridden, persons

confined to poorly ventilated homes without air
conditioning during summer heat waves
465 deaths in Chicago 1995 certified as heat related

Victims of CHS commonly suffer from chronic diseases,

alcoholism, or mental illness that predispose to heat
illness.
Patients are often taking anticholinergics,
antiparkinsonian drugs, or diuretics that impair the ability
to tolerate heat stress and therefore increase risk

Classic vs Exertional sx

Classic
Sweating often absent
ARF 5%
Respiratory alkalosis

Exertional
Sweating usually present
ARF 25-30%
rhabdomyolysis
Hypoglycemia
Coagulopathy
Lactic acidosis

Signs and symptoms

Dizziness
Altered mental status
Weakness
Nausea
Vomiting
Blurred vision
Convulsions
diarrhea

Syncope
Anhidrosis
Weak pulse
Hypotension
Hyperthermia
Constricted pupils

Lab findings
decreased Na, K, Ca, and PO4
Increased BUN
Hyperuricemia
Lactic acidosis
Leukocytosis
Hemoconcentration
Thrombocytopenia
Increased INR
Fibrinolysis

Consumption coagulopathy
Concentrated urine
Dehydration
proteinuria
Tubular casts
Myoglobinuria
Elevated AMIP
EKG changes
*** Elevated AST/ALT ***

Hepatic damage
Hepatic damage is so consistent a feature in

heat stroke that its absence should cast doubt

on the diagnosis
Patients often have no permanent impairment of
liver function.

Heat stroke- treatment

Secure the airway
Remove patients clothing
Monitor temp with rectal probe and UO with Foley
Immediate cooling with evaporative methods or
immersion (stop when body temp reaches <102.2 F)
Administer oxygen
Administer IVF with D5 1/2 NS or D5NS, or LR
Check glucose
CBC, CMP, AMIP, lactate, coags, DIC, ABG, UA

Immersion cooling
Fastest whole-body cooling rates and lowest mortality
rates have been observed with cool water immersion
Immersion in ice-water results in rapid reduction of core
temp to less than (102.2 F) within 10-40 minutes.
complications from hypotension and shivering in addition to
the possibility of ventricular fibrillation and the need for
defibrillation while in the water.
Vasoconstriction from ice-water immersion has proved
beneficial to hypotensive patients and may have benefits in
victims with shock who have poor peripheral circulation.

Evaporative cooling
Rapid and effective and easily performed in most

ER settings.
Patients clothing should be removed and the
entire body sprayed with water (~59 F) while
cooled or ambient air is passed across the
patients body with large fans.

Other cooling modalities

Preferred
Evaporative cooling
Ice-water immersion

Adjuncts
Ice packs
Cooling blanket
Rectal lavage
Gastric lavage
Cardiopulmonary bypass

antipyretics
Aspirin and acetaminophen are not indicated due to the
differing pathophysiology of heat stroke and fever
Salicylates

In large doses, may worsen hyperthermia by uncoupling

oxidative phosphorylation and aggrevating bleeding
tendencies

Acetaminophen
Can result in further hepatic damage

Secondary heat stroke

complications
Shivering
Convulsions
Myoglobinuria
Hypokalemia
hypocalcemia

shivering
Shivering

Greater potential with immersion methods

Chlorpromazine 25-50 mg IV (only if cooling is
inadequate due to vigorous shivering)
Has anticholinergic properties that may interfere with
sweating and may cause hypotension or precipitate
convulsions

convulsions
Convulsions

Diazepam 5-20 mg IV
Phenobarbital 130-260 mg initially IV

Acute renal failure

Myoglobinuria

Keep urine output > 50 mL/h

Mannitol 0.25 mg/kg or 12.5 gm IV initially, then 12.5
gm/L IVF
bicarbonate to alkalinize the urine

hypokalemia
Frequently accompanies heat stoke but may not

appear until rehydration.

Replace deficits cautiously

hypocalcemia
Treatment usually not necessary unless cardiac

manifestations are present.

Disseminated intravascular
coagulation- DIC
Hypofibrinogenemia
Elevated fibrin split products
Prolonged prothrombin time
Thrombocytopenia
Heparin for DIC remains controversial.

7500 U
q4hr has been efficacious in some studies.

Coagulation disturbances
May occur initially but commonly present on 2 nd

and 3rd days.

Initial treatment should be replacement with
fresh frozen plasma and platelets.

Prevention
Acclimatization

Achieved by scheduled regulated exposure to hot

environments and gradually increasing duration of
exposure and work load
Body adjusts by producing sweat with lower salt
concentration in greater amounts at lower ambient
temperatures
Also accompanied by increased plasma volume,
cardiac output, stroke volume, and slower heart rate.

Measurement of Environmental
Stress- Wet Globe Bulb Index

WBGT index = (0.7 Twb) + (0.2 Tg) + (0.1 Tdb)

Very high risk: WBGT above 28C (82F)
High risk: WBGT 23-28C (73-82F)
Moderate risk: WBGT 18-23C (65-73F)
Low risk: WBGT below 18C (65F)
Tdb air temp measured with a standard dry bulb thermometer not in
direct sunlight
Twb measured with a water-saturated cloth wick over a dry bulb
thermometer in direct sunlight (not immersed in water)
Tg measured by inserting dry bulb thermometer into a standard black
metal globe in direct sunlight

Prevention

Avoiding strenuous exercise if concurrent illness,

respiratory infection, diarrhea, vomiting, or fever.

Adequate ingestion of fluids prior to and during
activity at elevated temperatures.
Postponing events when WBGT is at high risk
category.

References

Armstrong, LE., et al. Heat and Cold Illness During Distance

Running. Medicine and Science in Sports and Exercise. 1996 28(12)
Chan, Theodore C., et al. Drug-induced Hyperthermia. Critical Care
Clinics 1997 13(4): 785-808.
Farci, et al. Harrisons Principles of Internal Medicine. 14th ed., New
York: McGraw-Hill Companies, Inc.
Rosen. Emergency Medicine: Concepts and Clinical Practice, 4th ed.
Mosby-Year Book, Inc. 1998.
Tierney, Lawrencence Jr., et al. Current Medical Diagnosis and
Treatment. 40th ed. New York: McGraw-Hill Company, Inc. 15431546.

The end