Dr.Viswanathan, MD

1. DR.VISWANATHAN, ASST PROF
INTERNAL MEDICINE, SRMC

2. OBJECTIVES OF THE SESSION
Thermoregulation- mechanisms and its responses in
hot and cold environments
Knowing about abnormal core temperatures in heat-
related illness and hypothermia
Clinical features of heat and cold related illness
Management

3. Thermoregulation
Normal set point of core temperature is 37 +/- 0.5
degree Celsius ( MODS- 41-43 degree C)

4. Heat loss mechanisms
1.Evaporation of skin moisture - single most efficient
mechanism of heat loss
Ineffective in high humidity ( >70%)
2.Radiation of infrared electromagnetic energy
3.Conduction- direct transfer of heat to a cooler
object
4. Convection-the loss of heat to air currents
Becomes ineffective when the environmental
temperature exceeds the skin temperature .

5. Responses in hot and cold
environment
Heat loss Hot environment Cold environment
Conduction Increased by
vasodilatation
Decreased by
vasoconstriction
Convection Increased Decreased
(* increased if wind
movement +)
Evaporation Increased by sweating
(* decreased if high
humidity)
Increased by
hyperventilation
Radiation Increased Decreased

6. Risk factors in heat illness
 Obesity
 Age extremes – young and elderly
 Poor conditioning and lack of acclimatisation
 Military personnel, laborers strenuously working in
heat
 Medical conditions – cardiovascular diseases
Medications - Anticholinergic agents impair sweating
Phenothiazines (anticholinergic properties ) interferes
with anterior hypothalamus due to central depletion
of dopamine affecting thermostat

7. Environmental Heat Problems
Normal body temperature range: 97.1 to 99.7 F (35-37 C)

8. Heat Related Disorders
Minor heat related
disorders
Heat rash
Heat edema
Hyperventilation
tetany
Exertion associated
collapse (Heat
syncope )
Major heat related
disorders
Heat cramps
Heat Exhaustion
Heat stroke

9. Heat Rash
Prickly heat (miliaria rubra)
Maculopapular erythematous rash in clothed areas
Predominant Sx- Itching
Blockage of the sweat pores by debris causes
inflammation and ducts dilate ----rupture and produce
superficial vesicles.
Rx Antihistamines, chlorhexidine
 Clothing should be clean and loose fitting

10. Heat Edema
Dependent edema in the hands, feet, and ankles
It is self limiting
Management: loosening clothes and elevating the
legs, diuretics are not indicated.
Involves cutaneous vasodilation and pooling of
interstitial fluid. Heat also increases the secretion of
ADH and aldosterone

11. Heat Tetany
Main cause is hyperventilation
Clinical features : Produces respiratory alkalosis
causing paraesthesias and carpo pedal spasm and
tetany
Management: removal from source of heat, and
controlling hyperventilation.

12. Exertion Associated Collapse (Heat syncope)
Mechanism: Decreased vasomotor tone, and
peripheral vasodilation causing postural hypotension
After removal from the heat source, most patients
will
recover promptly with cooling and rehydration.

13. Major Heat related illness

14. Heat Cramps
Intermittent, painful, and involuntary spasmodic
contractions of skeletal muscles.
Typically occur in an unacclimated individual who is
at rest after vigorous exertion in a humid, hot
environment
 No elevation of core temperature.
 D/t extracellular sodium depletion as a result of
persistent sweating, exacerbated by replacement of
water but not salt.
Symptoms usually respond rapidly to salt
replacement

15. Heat Cramps
Due to fluid and
electrolyte loss due to
sweating
Core Temperature
normal
Electrolyte drink

17. Heat Exhaustion
Physiologic hallmarks of heat exhaustion in
contrast to heatstroke are the maintenance of
thermoregulatory control and CNS function
Core temperature is elevated >37 C < 40 C
Inadequate salt and water replacement
Diagnosis of exclusion

18. Heat Exhaustion
Fluid and electrolyte loss
causing hypovolemia
Signs of shock!
Get out of heat
ABC’s
Treat for shock
Cooling measures
Electrolyte drink (if
airway secure)
Medical care/EMS)

20. Heat stroke
Total loss of thermoregulatory function.
Typical vital-sign abnormalities include
tachypnea,tachycardias, hypotension, and a widened
pulse pressure, anhidrosis
Triad :
1.Exposure to a heat stress,
2.CNS dysfunction, and
3. core temperature >40.5°C helps establish the
preliminary diagnosis

21. Exclude the following (DDs)
Sepsis including meningitis, cerebral abcess,
Malaria
Drug overdose- cocaine, amphetamines,
hallucinogens
Malignant hyperthermia/NMS
Thyroid storm
Pheochromocytoma

22. Clinical features:
Headache, nausea and vomiting.
Neurological manifestations: coarse muscle tremor ,
confusion, loss of consciousness.
The patient's skin feels very hot, and sweating is
often absent due to failure of thermoregulatory
mechanisms.
Complications:
Hypovolaemic shock, lactic acidosis, disseminated
intravascular coagulation(DIC), rhabdomyolysis,
hepatic and renal failure (MODS)

23. Heat Stroke (Hyperthermia)
Elderly, young, or
chronic illness
High temp and high
humidity
Hot dry skin
High body temp (above
105 F)
Rapid bounding pulse
Change in LOC
Seizures

24. Cooling tecniques
Spraying Cool water (15°C [60° F]) on exposed skin
 Fans direct continuous airflow over the moistened
skin.
 Cold packs applied to the axillae and groin
Safety of Immersion cooling (only for young,
previously healthy patients )

25. Other methods:
IV infusion of cold fluids
Cold irrigation of the bladder or GIT
Cold thoracic and peritoneal lavage (efficient
maneuvers but invasive )

26. Heat Stroke Treatment
Cooling measures
Crystalloids IV
Coagulopathy – FFP
and platelets
BZDs for sedation in
agitated patients

27. Cold related illness

28. Predisposing factors of hypothermia
Elderly
Chronic illness – CVA, parkinsons, spinal cord
injury
Malnourishment
Endocrine diseases: Hypothyroidism
Cortisol insufficiency
diabetes
hypopituitarism
Alcoholism and drugs ( phenothiazines,
sedatives)

29. Endocrine dysfunction leads to hypothermia
1.Hypothyroidism and myxedema coma reduces the
metabolic rate and impairs thermogenesis
2.Adrenal insufficiency and hypopituitarism increase
susceptibility to hypothermia.
3.Hypoglycemia - because of neuroglycopenic effects on
hypothalamic function.
4.Increased osmolality and metabolic derangements
associated with uremia, DKA and lactic acidosis can
lead to altered hypothalamic thermoregulation

30. Localized Cutaneous Cold Injury
Occur s at peripheral sites on the body
It classified into:
Freezing (Frostbite)
Nonfreezing (immersion)

31. Nonfreezing Cold Injury
 Trench Foot or Immersion Foot
 Less severe form of cold injury resulting from
prolonged exposure to cold and usually damp
conditions.
 Initially the limb (usually foot) appears cold, and
numb but there is no freezing of the tissue.

32. On rewarming the limb appears mottled, swollen and
painful.
Recovery may take many months
Probably involves endothelial injury
Gradual rewarming is associated with less pain than
rapid rewarming

33. Chilblains:
Tender red skin lesions
Self limiting
Often seen in swimmers, cyclists

34. Freezing Cold Injury- Frostbite
Direct freezing of body tissues
Usually affects the extremities, in particular the fingers,
toes, ears and face
Risk factors : smoking, peripheral vascular disease,
dehydration and alcohol consumption.
The tissues may become anaesthetised before freezing
and as a result the injury is often not recognised until
later, e.g. when boots are removed.

35. Frostbitten tissue is initially pale and doughy to the
touch and insensitive to pain.
Once frozen, the tissue is hard.
Amputations should be delayed for 2-3 months as
good recovery may occur over an extended period

36. Frostbite
Prevention is best
Get out of cold
Remove constricting
clothing
Immersion in warm water
( 37-39 degree C)
Analgesia as rewarming is
painful
Pentoxifylline
( vasodilator) improves
tissue survival

37. Frostbite - necrosis

38. Hypothermia
Hypothermia exists when the body's normal thermal
regulatory mechanisms are unable to maintain heat in
a cold environment and core temperature falls below
35°C

40. Investigations:
Haemoconcentration and metabolic acidosis are
common.
ECG may show characteristic J waves which occur at
the junction of the QRS complex and the ST
segment , VF may occur
AST and CK may be elevated due to skeletal muscle
damage
Serum amylase is elevated ( subclinical pancreatitis)
Although the arterial oxygen tension may be normal
when measured at room temperature, the arterial PO2
in the blood falls by 7% for each °C fall in core
temperature.

41. Management:
1.Rewarm the patient in a controlled manner
2.Treating the associated hypoxia, fluid and electrolyte
disturbance, and
3.Treating cardiovascular abnormalities, particularly
dysarhythmias

42. Mild hypothermia:
Sheltering the patient from the cold,
Replacing wet clothing, covering the head and
insulating him or her from the ground.
Patients should be maintained in a warm room, with
additional thermal insulation (blankets and/or space
film blanket).
Warm fluids to drink
Core temperature will rise slowly over a few hours
Underlying conditions should be treated e.g.
hypothyroidism with tri-iodothyronine 10 μg i.v. 8-
hourly

43. Severe hypothermia
In addition,
Supplementary oxygen,
warm intravenous fluids
 Monitoring of cardiac rhythm and arterial blood
gases, including H+
(pH) is essential.
 Active rewarming measures - administration of
warm humidified oxygen, lavage of the stomach,
peritoneal cavity or rectum with warm fluid,
haemodialysis and cardiac bypass.

44. Thank you