Complete description including diagnosis and management Contain both minor and major heat illnesses

1. HYPERTHERMIA AND
HEAT STROKE
DR DEEPAK KUMAR
ASSISTANT PROFESSOR
MAULANA AZAD MEDICAL COLLEGE
NEW DELHI, INDIA
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2. HYPERTHERMIA
• Rise in body temp. beyond the hypothalamic set point
• Due to inadequate loss and/or excessive heat gain.
• Failed Thermoregulation.

3. • What is Fever?
• How it is different from Hyperthermia?
To Differentiate, Lets first understand the Patho-
physiology of both.

4. PHYSIOLOGY OF
THERMOREGULATION

5. • THERMORECEPTORS IN
CORTEX
/HYPOTHALAMUS/MID
BRAIN/MEDULLA/SC/D
EEP ABDOMINAL
ORGANS
CORE TEMP.
• THERMORECEP
TORS IN SKIN
SHELL
TEMP.
LAT.
SPINOTH
ALAMIC
TRACT
TEMP.
CHANGE
SENSED
TEMP DIFF.
FROM SET
POINT
PREOPTIC
/ANTERIOR
HYPOTHAL
AMOUS
THERMOREG
ULATION
Thermoregulatory center
McAllen RM. Preoptic thermoregulatory mechanisms in detail. Am J Physiol Regul Integr Comp Physiol 2004;287(2):R272-3

7. FEVER
• Body’s defensive response
• Hypothalamic set point is raised
• Thermo-regulated elevation of body temp.
• Unfavourable environment for pathogens to grow
• High grade >40 C can be seen but remains briefly
followed by sweating

8. INFECTION/MICROBIA
L TOXIN//IMMUNE
REACTIONS
MONOCYTES/MACROPHA
GES/ENDOTHILAIAL CELLS
PYROGENIC
CYTOKINES(IL-1,IL-
6,TNF,IFN)
&MICROBIAL TOXINS
HYPOTHALAMIC
ENDOTHELIUM
PG E2CYCLIC AMP
ELEVATED
THERMOREGULATORY
SET POINT
HEAT PRODUCTION
&HEAT
CONSERAVATION
FEVER

9. HEAT LOSS HEAT GAIN
PHYSICAL ACTIVITY
BASAL METABOLISM
EMOTIONAL/HORMONAL
PASSIVE HEAT
CONDUCTION(3%)
CONVECTION (12-15%)
EVAPORATION(25%)
RADIATION(55-65%)
HYPER
THERMIA
Lee-Chiong TL Jr, Stitt JT. Disorders of temperature regulation. Compr Ther 1995;21(12):697-704

10. HYPERTHERMIA VS FEVER
HYPERTHERMIA FEVER
Setting Environmental
exposure/increased
production/decreased
dissipation
Infection
Temperature (>40 deg C/104 deg F)
common
(>40 deg C/104 deg F)
rare
Hypothalamic set point Not raised raised
Sweating Usually absent or minimal
but may be present
continuously
Profuse
Skin Dry /flushed Moist
Shivering Absent Present
Response to antipyretics Absent Marked

11. CELLULAR RESPONSE: COMPENSATED (HEAT ILLNESS)
SYSTEMIC INFLAMMATORY
RESPONSE
 LEVELS OF TNF- / IL-1/ IL-6
LEUKOCYTES/ENDOTHELIAL
CELLS/EPITHELIAL CELLS
CYTOKINES
CELL HEALING & REPAIR MODS
PREVENTED
CELL SURVIVAL RESPONSE
HEAT STRESS HEAT SHOCK
ELEMENTS
 TRANSCRIPTION OF HEAT SHOCK
PROTEINS
HSP= MOLECULAR CHAPERONES 
PREVENT PROTEIN DENATURATION
HSP ALSO MODULATE
BARORECEPTOR REFELXPREVENT
HYPOTENSION

12. CELLULAR RESPONSE:DECOMPENSATED (HEAT STROKE)
• 41-42 deg C TISSUE INJURY IN 1-8 HOURS
• DEHYDRATIONHYPOVOLEMIA  SWEATING
+ CUTANEOUS VASOCONSTRICTION
TEMPERATURE
• PROINFLAMMATORY MEDIATORS (TNF- /IL-
1/IFN-) DOMINATE OVER ANTI-
INFLAMMATORY MEDIATORS ( IL-10 / sTNF- )
• SIR  MODS
EXAGGERATED SIR
•  EXPRESSION OF ADHESION MOLECULES
PROYHROMBOTIC STATE
•  AT-3/ PROT C/ PROT S
ACTIVATION OF
COAGULATION
CASCADE
• ADVANCED AGE/ FAILURE TO
ACCLIMATIZE/GENETIC
INADEQUATE HSP
RESPONSE
• TRANSLOCATION OF ENDOTOXINS & RELEASE OF
PRO INFLAMMATORY CYTOKINES 
• ENDOTHELIAL ACTIVATIONNO & ENDOTHELIN
RELEASE  ALTER HEMODYNAMICS
GI ISCHEMIA

13. HYPERTHERMIA

14. CHILDREN
MORE PRONE TO
HYPERTHERMIA
GREATER BSA/MASS
RATIO
MORE HEAT
PRODUCED PER KG
BWT
SLOWER SWEATING
RATE
SWEATING STARTS
AT HIGHER TEMP
LOWER CARDIAC
OUTPUT
Bytomski, Jeffrey R., and Deborah L. Squire. “Heat illness in children..” Current Sports Medicine Reports 2, no. 6
(December 2003)

15. MECHANISMS AND CAUSES
MECHANISMS
OF
HYPERTHERMIA
EXOGENOUS
MECHANISMS
 HEAT
ABSORPTION
 HEAT LOSS
ENDOGENOUS
MECAHNISMS
 HEAT
PRODUCTION
 HEAT LOSS

16. INCREASED
EXOGENOUS
HEAT
ABSORPTION
HOT
CLIMATE
HOT
WORKSHOPS
DARK
CLOTHING
“FORGOTTEN
BABY
SYNDROME”

17. EXOGENOUS
HEAT
ABSORPTIO
N

18. DECREASED
EXOGENOUS
HEAT LOSS
HEAT
INSULATING
CLOTHING
MATERIALS
PROTECTIVE
EQUIPMENTS/
UNIFORMS
HIGH
HUMIDIDTY
INSUFFICIENT
VENTILATION
REDUCED
WIND

19. DECREASED
HEAT LOSS

20. ENDOGENOUS
INCREASED
HEAT
PRODUCTION
INTENSIVE
MUSCULAR
LOADING(EXERCISE)
PATHOLOGICAL
CONTRACTIVE
THERMOGENESIS
OXIDATION-
PHOSPHORYLATIO
N DISCONNECTION
(2,4 DNP
/SALICYLATE/HYPERTHYROI
DISM)
AUTONOMIC
DYSFUNCTION(S
S/SYMPATHOMI
METIC)

21. ENDOGENOUS
HEAT
PRODUCTION

22. DECREASED
ENDOGENOS
HEAT LOSS
DECREASED
SWEAT
PRODUCTION
(ANTICHOLINERGI
C)
SKIN VESSEL
SPASM(ADENOMIMETICS)

24. COMMONLY USED
ANTICHOLINERGIC
DRUGS
• Atropine
• Hyoscine
• Glycopyrrolate
• trihexyphenidyl
ADRENOMIMETIC DRUGS
• theophylline
• Caffeine
• Ketamine
• Ephedrine
• Amphetamines

25. HEAT ILLNESSES

26. DISEASE
SPECTRUM
1. HEAT
CRAMPS
2.PRICLY
HEAT
3.HEAT
TETANY
4.HEAT
EXHAUTION
5.HEAT
SYNCOPE
6.HEAT
EDEMA
MOST
SEVERE FORM
7. HEAT
STROKE

27. 1. HEAT CRAMPS
• Intermittent ,painful, spasmodic contraction
of skeletal muscles (Calf & hamstring)
• During / after vigorous exercise
• Hypotonic fluid + insuff. Na intake  hyponatremia prevent
Na gradient from being strong enough to power the Ca
pumps Ca ions remain in the myofibrils  muscle stays
contracted
• Oral rehydration and electrolyte replenishment

28. 2. PRICKLY HEAT ( MILIRIA RUBRA/SWEAT RASH/HEAT RASH)
• Macular /popular/vesicular, erythematous, pruritic rash
• Common @ clothed areas
• Blockage of sweat gland openings by stratum corneum debris
causing inflammation of sweat glands
• Ducts rupture vesicles risk of other major heat illness
increase(if large surface of the body involved) due to anhidrosis
in the affected region
• Loose & clean clothes + Antihistaminics

29. 3. HEAT TETANY
• Heat  hyperventilation  respi alkalosis  parsthesias
(extremities & circumoral) & carpopedal spasm
• High pH causes enhanced binding of calcium with proteins
iCa
• Can be differentiated from heat cramps as there is very little to
no pain
• Cooling

30. 4. HEAT EXHAUTION
• Illness with nonspecific symptoms.
• Common- General irritability, fatigue, weakness, light-headedness,
headache, nausea ,vomiting, and muscle cramps.
• accompanied by poor judgment, irritability, dizziness, making
differentiation from heat stroke difficult.
• Core temp. < 40 deg C

31. • 2 types -
• water depletion type
- lack of fluid intake + exertion in hot environment
-signs of hypovolemia predominate
• salt depletion type
- consumption of hypotonic fluids hyponatremia  neurological
features  seizures & coma
Most cases – mixed salt and water depletion

32. MANAGEMENT
Initial management – on site
• Discontinue motor activity
• Remove source of heat exposure
• Reduce clothing or equipment.
• Shift to a cool or air-conditioned space
• Place in Supine position Raise lower extremities slightly 
Venous return
• Oral rehydration therapy

33. Redrawn from Glazer JL: Management of heatstroke and heat exhaustion, American Family Physician

34. WHEN TO CONSIDER HOSPITALISATION?
• The symptoms of heat exhaustion mostly resolve
within 2–3 hours.
• If- Patient’s symptoms have not improved within the
first 20–30 minutes of the initial on site management.

35. • MANAGEMENT
Vital signs + core temp monitoring.
Monitoring core temperature- rectal.

36. Measuring rectal temp.
• Put petroleum jelly on the bulb end.
• Lay the child face down and spread the
buttocks apart.
• Insert the bulb end approx. 3 cm past the anal
margin.
• Held for at least 1 minute, or until the temp.
stopped rising.
Morley CJ. Axillary and rectal temperature measurements in infants. Arch Dis
Child. 1992 Jan;67(1):122-5.

37. Rectal and Esophageal thermometers

38. • Laboratory evaluation
Eletrolyte imbalances
Features of dehydration- elevated hematocrit and serum urea.
LFT, KFT, VBG- ?? Heat Stroke progression.
• Intravenous fluid and electrolyte replacement therapy is
employed.
• More aggressive cooling measures not warranted

39. Seen commonly in elderly patients
5. HEAT EDEMA
• Dependent extremities
• Due to cutaneous vasodilation + pooling of interstitial fluid
• Resolves within few days
• Diuretics NOT to be given  volume depletion
6. HEAT SYNCOPE
• prolonged stationary standing / sudden standing after prolonged heat
exposure
• Volume depletion + peripheral vasodilation + decreased vasomotor tone  
venous return causing cerebral hypoperfusion
• Elderly
• Fluids + cooling+ supine position

40. HYPERTHERMIA SYNDROMES

41. MALIGNANT HYPERTHERMIA
• Genetic syndrome (50% AD & 50% point mutation) - gene encoding
RYR1 ryanodine receptor
• The incidence of MH reactions ranges from 1:5,000 to 1:50,000.
• Neuromuscular disorders (muscular dystrophy, myotonia) high risk
• First signs- masseter spasm during ET intubation/ increase ETCO2
• Imp. in OT/intensive setting
Rosenberg, Henry et al. “Malignant hyperthermia.” Orphanet journal of rare diseases )

42. Management
• Immediate discontinuation of the possible trigger agent.
• The inspired gas is converted to 100% oxygen at a high flow rate to
wash out residual anaesthetic as rapidly as possible.
• The dantrolene, 2.5 mg/kg IV, is given as rapidly as possible.
• Cold normal saline, 15 mL/kg, is administered rapidly if the
temperature is >39°C
• Hyperkalemia

43. NEUROLEPT MALIGNANT SYNDROME
4 cardinal signs –
1. muscle rigidity
2. mental status change(confusion/ catatonia/ bradykinesia/
encephalopathy/ coma)
3. Hyperthermia
4. autonomic instability (labile hypertension /diaphoresis)
Neuroleptic agents - Haloperidol/ Chlorpromazine/ Fluphenazine/
Risperidone/ Clozapine/ Olanzapine)
• Promethazine and Metoclopramide are also implicated.

44. DOPAMINE
BLOCKADE
In
hypothalamus
alters central
thermoregulati
on
In basal ganglia 
muscle rigidity 
increased heat
production
In central
mesolimbic
regions 
altered
mental status
At level of
spinal cord 
dysautonomia

45. SEROTONIN SYNDROME
Triad – abnormalities of-
1. mental status (agitation / hypervigilance/ delirium)
2. neuromuscular function (clonus/ hyperreflexia)
3. autonomic function (hyperthermia/ tachycardia/ HTN/
diaphoresis/vomiting diarrhoea)
Develops within 24 hrs of drug admin
Overstimulation of 5-HT1A and 5-HT2A

46. Management
• Antidote- Cyproheptadine, a H1 receptor antagonist with
nonspecific serotonergic (5-HT1A and 5-HT2A) antagonistic
properties.
• Cyproheptadine (tablet or syrup).
• Total daily dose of 0.25 mg/kg divided every 6 hours.
• The maximum daily dose is 12 mg for children 2-6 years and 16 mg
for children 7-14 years old.

47. HEAT STROKE

48. Definition
• No universally accepted definition exists
• Bouchama’s definition (commonly used)
Core body temp. above 40 °C, accompanied by hot dry
skin and CNS abnormalities (delirium, convulsions &
coma)
Form of hyperthermia associated with SIR that leads
multi-organ dysfunction, predominantly
encephalopathy.
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002;346:1978–88

49. Features Bauchama Misset Pease JAAM Modified JAAM
Tempera
ture
> 40˚C >40.5°
C
>40.6 °C High environmental
temperature
High
environmental
temperature
CNS Encephalop
athy
delirium,
convulsions
& coma
Alteration
of mental
status
(coma,
delirium,
disorientati
on or
seizures)
Impaired
consciousness, Japan
Coma Scale score of
≥2 , cerebellar
symptoms,
convulsions, or
seizures)
Glasgow Coma
Scale (GCS) score
of ≤14
Sytemic SIR with
MOD
Hepatic/renal
dysfunction
Coagulation disorder
Creatinine or
total bilirubin
levels of ≥1.2
mg/dL
Skin Hot, dry
skin
Hot, dry, or
flushed skin

50. Classification
• Classic / Non-Exertional Heat Stroke.
• Exertional Heat Stroke.

51. Features Classic heat stroke Exertional heat stroke
Age group Prepubertal, elderly Post-pubertal and active
Occurrence Epidemic (heat waves) Sporadic (any time of year)
Activity Sedentary Strenuous
Health status Chronically ill Generally healthy
Medications Prescribed for chronic illness None/ illicit drugs
Mechanism Absorption of environmental heat
and poor heat dissipation
Excessie heat production,
which overwhelms heat-loss
Sweating Maybe absent (dry skin) Usually present (wet skin)

52. Epidemiology
• “Silent disaster” - develops slowly and kills humans
and animals nationwide.
• > 22,000 fatalities in India (1992-2015).
• In 2015, the country witnessed the fifth deadliest
heat wave in history.
2300 deaths – in Andhra pradesh., Telangana,
Punjab, Odisha, Bihar
• June 2019- 53.96% population exposed to heat
waves
National Disaster Management Authority. GOI. 2017

53. Deaths in India

54. Deaths due to significant heat waves
worldwide

55. Heat Wave
• Condition that leads to physiological stress and can
cause death due to rise in atmospheric temp.
• World Meteorological Organization
Daily max. temp. exceeds the avg. max. temp. of
the area by 5° C for 5 consecutive days.
Or if the max temp. of any place continues to >45°
C consecutively for 2 days. (Costal >40)

57. Heat index / Apparent temperature
• What the temp. feels like to the body when the
humidity is combined with the air temp.
• When the humidity is high, rate of perspiration
decreases and the body feels warmer.
• Ex- if air temp. is 34°C and relative humidity is 75%,
the heat index--how hot it feels--is 49°C.
The same effect is reached at just 31°C when the
relative humidity is 100 %.

59. • Mortality from heat stroke has been reported to
increase due to climate change
• By the 2050s, heat stroke-related deaths are
expected to rise by nearly 2.5 times
• 25-50% mortality even with aggressive care

60. HEAT
STROKE
SIR MOD DIC

61. Clinical features
• History of Heat exposure/physical exertion
• Multi-system involvement-
• CNS
Irritability, delirium, encephalopathy, coma.
• GIT
Nausea, Vomiting, Pain Abdomen, Jaundice,
melena

62. CVS
• Tachyarrhythmias and hypotension are common.
Respiratory
• Tachypnea, Distress, Hemoptosis (Edema, ALI, ARDS)
Hematological
• Rashes, Bleed from various sites (Consump.
Caugulopathy and Liver Failure)

63. Symptoms Kaleiselvan(%
symptomatic)
Lakhotia Argaud et al.
No.
Age
26
53+/- 22
102.7+/-2.7
40
42 +/-3
102.2 2.5
83
79.6 ± 9.9
106 ± 2.34
CNS
Disoriented
Drowsy
Coma
Seizures
All
50
11
34
30
All
50
10
36
32
All
56
3.6
GIT
Nausea and Vomiting
Diarrhea
30
30
15
Resp Failure
(Mech Vent)
26 (100%) 47 (60%)
Cardiovascular
Shock (vasopressor)
23 43
Renal (AKI) 57 34
Hepatic 34 2.4
Hematological 26 3.6
35% 64%30%

64. Close Differentials
• CNS- Meningitis, Encephalitis
• Infection- Sepsis, Malaria
• Grave Disease, Thyroid storm
• Drug withdrawals- Narcotics, Benzodiazepines

65. Laboratory evaluation
Test Findings Interpretation
Blood Leukocytosis Systemic inflammation from
(heat-related illness or
sepsis)
Elevated hematocrit Dehydration
Thrombocytopenia,
elevation in hyper-
segmented neutrophils, and
atypical lymphocytes
heat injury
Electrolytes Hyponatremia
Hypernatremia
hyperkalemia
hyperphosphatemia, and
hypocalcemia
Loss in sweat
Dehydration
Muscle damage
Glucose Hypoglycemia Fulminant hepatic failure

66. LFT Elevation in AST and ALT Liver dysfunction
KFT Deranged KFT AKI
Urine Proteins Rhabdomyolysis
Myoglobulin Rhabdomyolysis
Increased sp. gravity Hypovolemia
CSF Nonspecific pleocytosis
CSF protein elevated
Given in National GUIDE
Animal model studies.
ABG Metabolic acidosis
Respiratory alkalosis
Lactic acidosis
CNS stimulation-
hyperventilaton

67. Coagulation studies Elevated PT-INR, APTT (DIC)
Creatinine kinase Raised (Muscle injury)
Chest X ray ARDS
Neuroimaging Cerebral infarction, hemorrhage, or
edema
ECG Arrhythmias

68. ECG Changes
• Seen in 85% of HS patients in one study.
• sinus tachycardia (43-79%)
• QT prolongation (61%)
• Both non-specific and specific ST changes associated
with coronary artery territories
• conduction defects- incomplete and complete RBBB
Mimish L. Electrocardiographic findings in heat stroke and exhaustion: A study on Makkah pilgrims.
Journal of the Saudi Heart Association. 2012; 24(1): 35-9 12.
Akhtar MJ, al-Nozha M, al-Harthi S & Nouh MS. Electrocardiographic abnormalities in patients with
heat stroke. Chest. 1993; 104(2): 411-4

69. Neuroimaging
MRI-
• selective vulnerability of cerebellar Purkinje cells to
heat-induced injury
• Ischemia/Hemmorhage in dentate nuclei, cerebellar
hemispheres, cerebellar peduncles, midbrain,
thalami, hippocampi, basal ganglia, the splenium,
temporo-occipital lobes
• Cerebral Edema
• Cerebral atrophy ( Late – after 2 weeks, Progressive)
Albukrek D, Bakon M, Moran DS, Faibel M, Epstein Y (1997) Heat-strokeinduced cerebellar atrophy: clinical
course, CT and MRI findings. Neuroradiology 39: 195–197
Sudhakar PJ, Al-Hashimi H (2007) Bilateral hippocampal hyperintensities: a new finding in MR imaging of heat
stroke. Pediatr Radiol 37: 1289–1291

70. TREATMENT

71. PRINCIPLES
• FIRST COOL THEN SHIFT
• RAPID COOLING METHOD HAS TO BE USED
• INTENSIVE CARE UNIT
• MOD MONITORING AND ORGAN SPECIFIC
TREATMENT

72. • Deaths has been seen as early as within 30 minutes
of heat stroke onset.
• start effective cooling method with min. rate of
0.20 C/ min.
• End point used in large series is 39 C (proven safe)

73. COOLING METHODS
COOL WATER IMMERSION
EXTERNAL COOLING
METHODS
INTERNAL COOLING
METHODS
CONDUCTION METHOD
EVAPORATION AND
FANNING
COOL IV SALINE
GASTRIC LAVAGE
BLADDER/BOWEL
IRRIGATION
BODY COOLING UNIT

74. External cooling methods

75. Whole body cold water immersion
• Most effective method of cooling
• Rapid rate of cooling
Ice used in water (1 C) – 0.35 C/min
Cold Water (5 C)- 0.15 C/min
• Immersion of only torso and legs- 0.25 C/min
level of neck- 0.35 C/min
hands and legs- 0.15 C/min
recommended - National Athletic Trainers’ Association and American College of Sports Medicine

76. TEMP
MONITOR
EQUIPMENT
/DRUGSHOLDING
BODY
HOLDING
NECK
VITALS
MONITOR

77. ?? Peripheral vasoconstriction
• Thought previously – immersion of body to cold water
– per vasoconstriction and shivering ( heat
production)
• Recent studies shown
a) Thermogenesis via shivering occurs in
normothermic not hyperthermia. (1)
b) if +, do not impede the cooling process (2)
1. Proulx CI, Ducharme MB, Kenny GP. Effect of water temperature on cooling efficiency during
hyperthermia in humans. J Appl Physiol. 2003;94(4):1317–1323
2. Casa DJ, McDermott BP, Lee E, Yeargin SW, Armstrong LE, Maresh CM. Cold-water immersion: the
gold standard for exertional heat stroke treatment. Exerc Sport Sci Rev. 2007;35(3):141–149

78. Disadvantages
• Whole setup is cumbersome
• More man power required
• Difficult to maintain IV access/vitals monitoring
• CPR if needed, cant be performed
• Patient can vomit, pass stool/urine

79. Evaporation and fanning
• Less efficient c/w cold water immersion
• Rate of cooling- o.15 C/min
• Body exposed- mist sprayer filled with cold water is
sprayed all over the body- continued with air fan @
min 0.5 m/s.
• If sprayer is not available, cold towels can be used.
Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A
Systematic Review. Journal of Athletic Training 2009;44(1):84–93

80. Cooling by ice packs
• Conductive cooling by the application of crushed ice
or ice packs to the body
• strategic application of ice packs to the axilla, neck,
and groin
• Rate of cooling- 0.028 C/m
• When applied to whole body- 0.034 C/m
• Ineffective method- takes 110 minutes to cool a
patient from 42.2C (108F) to 38.9C (102F)
Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A
Systematic Review. Journal of Athletic Training 2009;44(1):84–93

83. Combined Ice pack+ evaporation+
fan
• Rate of cooling – 0.175 C/m

84. Body-cooling unit (BCU),
• Specially constructed device, produces a superior
cooling rate of 0.31 ˚ C/min
• Directing air currents while simultaneously spraying
water on patients
• Cost- 18,000 USD!!!
Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced Hyperthermia: A
Systematic Review. Journal of Athletic Training 2009;44(1):84–93

85. Body Cooling Unit

86. Cold External Environment
• Bring the patient away from the exposure
• Preferably to the cool area (ac units)
• Rate of cooling – 21 C/ 20% humidity- 0.06
32 C/ 20% humidity-0.02
• management in an ICU without ac were
independently associated with an increased risk of
hospital death
Misset B et al. Mortality of patients with heatstroke admitted to intensive care units during the
2003 heat wave in France: a national multiple-center risk factor study. Crit Care Med. 2006;34:
1087–92.

87. Internal cooling method
Include gastric, peritoneal, and bladder lavage with
cold water.
• Rate of cooling- 0.018 C/min
• Role not been fully established
• Can be used along with other methods
Brendon P. McDermott et al. Acute Whole-Body Cooling for Exercise-Induced
Hyperthermia: A Systematic Review. Journal of Athletic Training 2009;44(1):84–
93

88. Other cooling methods
• Intravascular balloon catheter cooling
• Rate of cooling - 0.12 C/min
• Inbuilt thermistor for sensing core body temp and
fluid infused
• change in temp. as small as 0.1°C sensed
Hamaya H1 et al. Successful management of heat stroke associated with multiple-organ dysfunction
by active intravascular cooling. Am J Emerg Med. 2015 Jan;33(1):124.

89. Intravascular balloon-catheter system

90. Extracorporeal Cooling

91. Medications
Dantrolene: Impairs calcium release from the
sarcoplasmic reticulum
• Reduces muscle excitation and contraction
• Studies show no difference in cooling rate, outcome,
mortality
Antithrombin III, rsThrombomodulin α:
• To treat coagulopathy??
• No proven studies
Eran Hadad et al. Clinical review: Treatment of heat stroke: should dantrolene be
considered? Crit Care. 2005; 9(1): 86–91
Hagiwara S et al. Highdose antithrombin III prevents heat stroke by attenuating
systemic inflammation in rats. Inflamm Res. 2010;59:511–8.

92. Poor prognostic factors
• Core temp > 40 C- bad, > 42 C - worst
• Duration of illness, > 60 min- bad, >90 min – worst
• Age - > 80 yrs, no pediatric data.
• Associated Heart disease or Malignancy
• Anuria, Coma
• On Diuretic therapy
• Use of Ionotropes within first 24 hours in ICU
• Management without Ac in ICU
• Increased PT, Raised ALT > 1000
Hausfater et al. Prognostic factors in non-exertional heatstroke. Intensive Care Med. 2010;36: 272–80.
Misset B et al. Mortality of patients with heatstroke admitted to intensive care units during the 2003
heat wave in France: a national multiple-center risk factor study. Crit Care Med. 2006;34: 1087–92

94. At site other than health center
• Remove clothing, cool water& fan skin.
• Place ice packs.
• Offer cool fluids if alert and able to drink
• Immediately transfer to nearest health care facility
• While transferring, cooling has to be contd.
• Start intravenous fluids.

95. AT HEALTH CENTRE
STEP 1
• Clinical assessment for CVS, Resp & CNS func.
• Exclude other D/D.
• Assess airway and ensure good resp. efforts.
• Put oxygen, IV lines take samples.
• Check body core temp. - rectal or esophageal.
• Send ICU call, start and continue treatment

97. STEP-2. Initiate cooling process
• Removal of body clothing
• Use mist fan / air conditioned room / Stand fans
• Ice packs at groins, neck and axilla, spray cool water
• Ongoing tepid sponging
• Lavage with cold saline via NG tube or urinary
catheter

99. STEP 3.
• Cooling can be stopped – 39 C
• Use Benzodiazepines for seizures.
• DO NOT use PCM or other NSAIDS.
• Close monitor- Core temp, BP, 4 hourly Dx, Hourly
Urine output, ECG, half hourly GCS

100. Step 4
• Seek and trace investigation results
• Look for signs of coagulopathies, AKI and liver
dysfunction
• ABG regularly – look for metabolic acidosis
• Most important!!!!

101. Inform / communicate with attendant
regarding patient condition

102. Prevention

103. THANKS