1. Hypothermia
David Caro, MD
University of Florida
Emergency Medicine

2. Introduction
 Definition
 Etiology
 Epidemiology
 Physiology
 Impact on organ systems

3. Introduction (cont’d)
 Response of organ systems
 Identification
 Treatment modalities
 Sequelae
 Review

4. Physiology
 The hypothalamus is your
temperature control center
 Core and peripheral receptors
provide temperature information
 Various responses help maintain
temperature homeostasis
 Cut heat loss; generate heat!

5. Physiology – Heat
Generation
 Basal Metabolic Rate = 40-60
Kcal/m2
 Movement, shivering can increase
the BMR 2 to 5 x normal

6. Physiology: The physics
of temperature
homeostasis
 4 ways heat is lost
 Radiation (65%)
 Evaporation (25%)
 Convection (5-10%)
 Conduction (2-5%) (except in
immersion; cold water conductivity
32 times that of air)

7. Physiology
 Our body responds to decreased
temperature by attempting to:
 Decrease heat loss
 Vasoconstriction
 Behavior modification
 Increase heat production
 Shivering
 Am J Physiol 1997 Feb;272(2 Pt
2):R557-62

8. Hypothermia-Definition
 A core body temperature below
96.8oF
 Mild hypothermia = 92 – 96.8oF
 Moderate = 88 – 92oF
 Severe = < 88oF
 “They’re not dead until they’re
warm and dead.” One case report
of recovery after accidental 15.2oC
(59.4F) hypothermia.

9. Hypothermia –
Morbidity/Mortality
 Mild hypothermia – very little
 Moderate – one study showed a
mortality rate of 21% for moderate
hypothermia

10. Clinical features
 Mild: shivering, loss of fine motor
control
 Moderate: lethargy, confusion
 Severe: pupillary dilation, coma,
cardiovascular irritability and
eventual collapse

11. Hypothermia
Etiology Overview
 Increase in heat loss
 Decrease in heat production
 Thermoregulatory failure

12. Etiology
Increased Heat Loss
 Exposure to ambient temperature
drop
 Trauma
 Alcohol/drugs
 Cutaneous vasodilation, impaired
shivering, decreased awareness of
environment , Wernicke’s
encephalopathy (Eur J Appl
Physiol 1996;74(3):293-5. Also,
Ann Neurol 1981 Oct;
10(4):384-7)

13. Etiology
Increased Heat Loss
 Exposure (cont’d)
 Sports
 Altitude

14. Etiology
Increased Heat Loss
 Exposure (cont’d)
 Immersion
 Significant risk begins in water colder than
25 C (72 F). The water temperature of
Lake Huron is approximately 4.6 C (40 F)
in May and is highest in August at 19 C
(66 F).
 Hypothermia can occur rapidly during
cold-water immersion (one hour or less
when water temperature is below 45oF).
 Core temp drops 0.3C in 20 min when
immersed in 22C (Am J Phys Med
Rehabil 1999 Jan-Feb; 78(1):33-8.

15. Etiology
Decreased Heat Production
 Acute Illness
 Metabolic abnormalities
 DKA
 Hypoglycemia
 Myxedema coma
 Hypoadrenalism

16. Etiology
Impaired Thermoregulation
 Sepsis
↓ lymphocyte activation
 ↓ IL-1,2,6 (Anesthesiology 1998
Nov; 89(5):1133-40. J
Neurotrauma 1999 Mar; 16(3):
225-32)
 CVA
 Autonomic dysfunction

17. Impact on Organ
Systems
 Respiratory
 Altitude will decrease pO2
 Temperature of inspired air
decreased
 Airwarmed + humidified by
oral/nasal mucosa prior to hitting
lower airways
 Expired air rich in warm water –
heat lost

18. Impact on organ
systems
 Hemoglobin increasingly binds O2
as temperature drops
(oxyhemoglobin dissociation curve)
 Hypoxia may occur due to
decrease offloading of oxygen
(Cardiovasc Surg 1999
Jun;7(4):425-31

19. Organ System Response
 Acid-base balance
 11/18 with decompensated
metabolic acidosis (Coll Antropol
1999 Dec;23(2):683-90
 Most texts recommend not
correcting for temperature when
evaluating ABGs

21. Impact on Organ
Systems
 Cardiac
 Repolarization becomes abnormal
with decreasing temperature
 Osborn Wave – lead V3 or V4
 Increasing cardiac irritability with
decreasing temperature
 QT prolongation (0.45-0.688 vs.
0.343-0.444; Coll Antropol 1999
Dec; 23(2):683-90)

22. Osborn Wave
 86% of hypothermic patients (Acad
Emerg Med 1999 Nov;
6(11):1121-6)
 Voltage gradient due to action
potential notch in epicardium;
epicardium activated later, which
manifests as notching or J-point
elevation (Circulation 1996 Jan
15;93(2):372-9)

24. Impact on Organ
systems
 Cardiac
 Mild: Tachycardia, hypertension,
increased CO
 Moderate: Bradycardia,
Arrhythmias
 Severe: Arrhythmias, hypotension,
decreased cardiac output
 Below 30C, ventricular fibrillation
risk increases

25. Impact on Organ
Systems
 Neurologic
 Decreasing metabolic activity of
neurons; therefore, decreased O2
requirement
 Linear decrease in CNS function
as temperature decreases
 Neuron function stops below 20C

26. Organ System Response
 Neurologic
 Decline in mental status
 Mild confusion
 Delirium
 Coma
 Peripheral anesthesia
 Ataxia

27. Impact on Organ
Systems
 Renal
 Hypothermia impairs renal
concentrating abilities
 “Cold-induced diuresis”
 Potential rhabdomyolysis → ATN

28. Impact on Organ
Systems
 Gastrointestinal
 Pancreatitis ± pancreatic necrosis
can develop due to HT

29. Impact on Organ
Systems
 Hematologic
 Hemoconcentration
 Increased blood viscosity
 Decreased flow in capillaries
 Potential for thrombosis
 Potential for DIC

30. Impact on Organ
Systems
 Musculoskeletal
 Temperature extremes can cause
crystallization of blood in
capillaries of extremities
 Cutaneous vasoconstriction occurs
in response to lower ambient
temperature

31. Organ System Response
 Musculoskeletal
 Frostbite
 Gangrene

32. Frostbite
 Grade as burns
 1st degree
 Erythema, edema, burning
 Swelling for ten days or more
 Desquamation
 Parathesias, aching, and necrosis
of the pressure points of the foot
 Increased sensitivity to cold,
hyperhydrosis

33. Frostbite
 Grading
 Second degree
 progresses to blister formation,
anesthesia, and deep color change

34. Frostbite
 Third degree
 involvesfull skin thickness and
extends into the subcutaneous
tissue
 Subfascial pressure increases;
compartment syndromes are
common

35. Frostbite
 4th degree
 Destruction of entire thickness
 Cyanotic, insensitive; hemorrhagic
blister formation.
 Severe pain on rewarming
 Dry gangrene can progress quickly
with mummification.
 The line of demarcation becomes
obvious at 20-36 days and extends
into the bone in 60 or more days.

36. Trenchfoot
 Caused by prolonged exposure of the
feet to cool, wet conditions.
 The skin is initially reddened with
numbness, tingling pain, and itching then
becomes pale and mottled and finally
dark purple, grey or blue.
 If circulation is impaired for more than 6
hours there will be permanent damage to
tissue.
 If circulation is impaired for more than 24
hours the victim may lose the entire foot.

37. Hypothermia
Identification
 Thermometry
 Most thermometers’ lower
temperature limit is 93oF
 A special low-temperature-reading
thermometer is necessary to read
temperatures lower than 93

38. Evaluation
 ABCDEs are the priority
 Handle patients gently
 Begin passive rewarming
immediately
 Cautious ACLS care (coming up)

39. Evaluation
 History is essential
 Environment/exposure
 PMH
 Medications
 Exam – be complete!
 Rectal temperature!
 Vital signs

40. Evaluation
 Head-to-toe secondary exam
 Neuro exam important – especially
cranial nerves (Wernicke’s)
 CV exam
 Extremities/nose/ears/other end-
arterial places

41. Evaluation
 Testing
 Cardiac monitor, EKG
 SaO2, ±ABG
 Electrolytes, CBC
 UA
 If severe:
 LFTS, PT/PTT, CK (rhabdo)

42. Treatment
 General Rx for various degrees of
hypothermia
 Specific Rx for sequelae
 CV
 Respiratory
 ATN/Rhabdo
 Frostbite/gangrene

43. Treatment Modalities –
Mild hypothermia
 Warm room
 Cover with dry, warm blankets
 Radiant warming
 Warmed p.o. fluids

44. Treatment Modalities –
moderate hypothermia
 ABCs – every patient
 Airway, Breathing – warm,
humidified air by ETT or NRBfm
 Circulation – IV access; warmed
crystalloid
 All of the above
 Bear Hugger

45. Treatment Modalities –
Severe Hypothermia
 All of the above
 Invasive modalities
 NG, foley lavage
 Pleural, peritoneal lavage
 Dialysis or Cardiac bypass

46. Treatment Modalities
How effective are they?
 Reflective Foil – 0.3C/hr Ann Emerg Med
2000 Apr; 35(40):337-45
 Warmed IVF – 1.0C/hr J Clin Anesth
1998 Aug;10(5):380-5.
 Warm IVF, Warm/humdified oxygen,
blankets – 1.4 C/hr Ann Emerg Med
1996 Apr;27(4):479-84
 Bear-Hugger – 0.7C/hr Ann Emerg Med
2000 Apr; 35(40):337-45; IVF/humidified
O2/BH – 2.4C/hr Ann Emerg Med 1996
Apr 27(4):479-84

47. Treatment Ideas
 Aviat Space Environ Med 1992
Dec;63(12):1070-6
 Total immersion in 42C bath – 10.2C/hr
 Blankets – 0.2C/hr
 J Appl Physiol 1998 Nov;85(5):867-8
 Subatmospheric pressure to limbs while
applying warm-water blanket increased
rewarming 10-fold over WWB alone
(13.6C/hr vs. 1.4C/hr)

48. Treatment modalities-
Sequlae
 Ventricular Fibrillation; MI
 Renal Failure
 DIC
 Frostbite
 Gangrene
 Afterdrop

49. Afterdrop
 Paradoxical drop in core temp
during rewarming
 Due to influx of cold blood from
periphery
 Can precipitate arrhythmias

50. Treatment of sequelae
 Ventricular fibrillation
 Cold heart very irritable
 Will not respond to multiple rounds
of drugs
 Shock – 3 times, then wait until
warm
 Bretylium your drug of choice
(ACLS Guidelines)

51. Treatment of sequelae
 Renal Failure
 Rhabdomyolysis : force fluids;
alkalinization
 Cold-diuresis : fluids, watch
electrolytes

52. Treatment of sequelae
 Frostbite
 Narcotics!
 Warm water immersion – warm,
wet heat is best.
 Do NOT warm then allow to
refreeze. Better to keep frozen
until definitive care is available.

53. Treatment of sequelae -
Afterdrop
 Try to avoid – aggressive
rewarming
 Expect arrhythmias, be prepared to
treat

54. Hypothermia
Summary
 Physiology plays a HUGE role
 Etiology
 Treatment
 History is key
 Rectal temp with low-reading
thermometer
 Treat temperature aggressively,
but handle patient gently
 Watch for afterdrop!

55. Text References
 Ann Emerg Med 1993 Feb;22(2
Pt 2):370-7
 Wilderness Medicine – Auerbach
 Rosen’s Principles of
Emergency Medicine