Navy Environmental Health Center
Technical Manual NEHC-TM-OEM 6260.6A June 2007
PREVENTION AND
TREATMENT OF HEAT AND
COLD STRESS INJURIES
NAVY ENVIRONMENTAL HEALTH CENTER
BUREAU OF MEDICINE AND SURGERY
PREVENTION AND TREATMENT OF HEAT AND COLD
STRESS INJURIES
Published By
Navy Environmental Health Center
620 John Paul Jones Circle, Suite 1100
Portsmouth, Virginia 23708-2103
June 2007
FOREWORD
This document will be regularly updated. The latest version may be found on the Navy
Environmental Health Center, Occupational and Environmental Medicine Directorate Web site at
the following Internet address.
http://www-nehc.med.navy.mil/occmed/index.htm
Reviewed and Approved
_____________________________________
W. R. Stover, CAPT, MSC, USN
Commanding Officer
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
i
Table of Contents:
CHAPTER 1:................................................................................................................................. 1
C1. INTRODUCTION.................................................................................................................. 1
CHAPTER 2:.................................................................................................................................
2
C2. PHYSIOLOGY OF HEAT STRESS....................................................................................
2
C2.1. Heat Transfer and the Human Body.................................................................................. 2
C2.1.1. Heat Equation............................................................................................................. 2
C2.1.2. Heat Dissipation (Removal)....................................................................................... 2
C2.1.2.1. Sweating (Perspiration).......................................................................................
2
C2.1.2.1.1. Skin Heat, Moisture, and Texture ................................................................
3
C2.1.2.1.2. Blood Shunting............................................................................................. 3
C2.1.2.1.2.1. Thirst ..................................................................................................... 3
C2.1.2.1.2.2. Drinks.................................................................................................... 4
C2.1.2.1.2.3. Intravenous Rehydration ....................................................................... 5
C2.1.2.1.2.4. Water Absorption .................................................................................. 5
C2.1.2.1.3. Sodium (Salt)................................................................................................ 5
C2.2. Environmental Heat Stress Factors ................................................................................... 6
C2.2.1. Measurement of Temperature .................................................................................... 6
C2.2.2. Wind........................................................................................................................... 6
C2.2.3. Humidity..................................................................................................................... 6
C2.2.3.1. Heat Index ........................................................................................................... 6
Figure 1- Heat Index Equation................................................................................ 7
C2.2.3.1.1. Physiologically Equivalent Temperature ..................................................... 7
C2.2.4. Rain ............................................................................................................................ 7
C2.2.5. Sun Position and Time of Day ................................................................................... 7
C2.2.6. Elevation..................................................................................................................... 8
C2.3. Individual Heat Stress Factors........................................................................................... 8
C2.3.1. Sunburn ...................................................................................................................... 8
C2.3.2. Clothing and Personal Protective Equipment (PPE)..................................................
8
C2.3.3. Illness ......................................................................................................................... 8
C2.3.4. Immunizations (Vaccinations, Inoculations).............................................................. 8
C2.3.5. Prior Heat Stress Injury..............................................................................................
9
C2.3.6. Recent Heat Stress Exposure......................................................................................
9
C2.3.7. Size............................................................................................................................. 9
C2.3.8. Population Characteristics.......................................................................................... 9
C2.3.9. Gender ........................................................................................................................ 9
C2.3.10. Age .........................................................................................................................
10
C2.3.11. Race........................................................................................................................ 10
C2.3.12. Acclimatization ......................................................................................................
10
Table 1 - Percent Optimum Heat Acclimatization................................................ 12
C2.3.13. Hydration Status..................................................................................................... 12
C2.3.13.1. Eu-, Hypo-, De-, and Hyper-hydration ........................................................... 12
C2.3.13.1.1. Euhydration ..............................................................................................
12
C2.3.13.1.2. Hypohydration..........................................................................................
12
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
ii
C2.3.13.1.3. Dehydration.............................................................................................. 12
C2.3.13.1.4. Hyperhydration......................................................................................... 12
C2.3.13.2. Water Intoxication........................................................................................... 13
C2.3.13.3. Hydration Status and Performance..................................................................
13
C2.3.14. Medications, Including Prescription and Non-Prescription Medications, Drugs of
Abuse, Folk Remedies, and Dietary Supplements................................................................
13
C2.3.15. Alcohol................................................................................................................... 14
C2.3.16. Activity, Rest, and Sleep........................................................................................ 14
Table 2 - Work-Rest Cycles and Fluid Replacement for 4 Hour Periods.............
15
C2.3.16.1. PHEL Curves...................................................................................................
15
Figure 2 - PHEL Curves ....................................................................................... 16
Table 3 - Safe Exposure Times Aboard Ship........................................................ 17
C2.3.16.2. Flag Conditions and Activity Limitations....................................................... 18
Table 4 - Flag Conditions and WBGT..................................................................
18
C2.3.16.3. Screening criteria for Heat Stress Exposure Ashore .......................................
18
Table 5 - Screening Criteria for Heat Stress Exposure (ACGIH) based on WBGT
............................................................................................................................... 19
C2.3.16.4. Muscle Performance in Heat Stress conditions............................................... 19
C2.3.16.5. Sleep Deprivation and Heat Tolerance............................................................ 19
C2.3.17. Mean Metabolic Rate ............................................................................................. 19
C2.3.18. Attributes of Surrounding Materials ...................................................................... 19
C2.3.19. Motor Vehicles....................................................................................................... 19
C2.3.20. Electric Blankets .................................................................................................... 19
C2.4. Heat Stress Vs. Heat Strain ............................................................................................. 20
C2.4.1. Heat Stress................................................................................................................ 20
C2.4.2. Heat Strain................................................................................................................ 20
Figure 3 - J Wave Appearance on Electrocardiogram.......................................... 20
Figure 4- Upper Limits of Exposure for Unimpaired Mental Performance ......... 21
C2.5. Prevention Of Heat Stress Injuries.................................................................................. 21
C2.5.1. Primary Prevention................................................................................................... 21
C2.5.2. Secondary Prevention...............................................................................................
21
C2.5.3. Tertiary Prevention................................................................................................... 22
Table 6 - Heat Stress Injuries—Risk Factors and Predisposing Conditions.........
23
C2.6. Temperature Measurement And Thermometers .............................................................
23
C2.6.1. Skin Temperature ..................................................................................................... 23
C2.6.2. Expired Breath.......................................................................................................... 23
C2.6.3. Oral Thermometers ..................................................................................................
23
C2.6.4. Tympanic (Ear) Electronic Thermometers............................................................... 24
C2.6.5. Rectal Temperature ..................................................................................................
24
C2.6.6. Esophageal Thermometers ....................................................................................... 24
C2.6.7. Bladder Temperature................................................................................................ 24
CHAPTER 3:...............................................................................................................................
25
C3. DIAGNOSIS OF HEAT STRESS INJURIES................................................................... 25
Figure 5 - Acute Heat Exposed Patient Diagnostic Flow Chart ...........................
26
C3.1.1. Heat Rash (Miliaria Rubra)......................................................................................
27
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
iii
C3.1.2. Erythema Ab Igne (Erythema Caloricum) ............................................................... 27
C3.1.3. Exertional Hyperthermia.......................................................................................... 27
C3.1.4. Heat Syncope............................................................................................................ 27
C3.1.5. Heat Edema ..............................................................................................................
28
C3.1.6. Heat Tetany ..............................................................................................................
28
C3.1.7. Heat Cramps............................................................................................................. 28
C3.1.8. Heat Exhaustion ....................................................................................................... 28
C3.1.8.1. Symptoms of Heat Exhaustion.......................................................................... 28
C3.1.8.2. Sodium-depletion Heat Exhaustion...................................................................
29
C3.1.8.3. Water-deficient Heat Exhaustion ......................................................................
29
C3.1.9. Heat Stroke............................................................................................................... 30
C3.1.9.1. Classic Heat Stroke ........................................................................................... 30
Table 7 - Risk Factors for Classic Heat Stroke..................................................... 30
C3.1.9.2. Exertional Heat Stroke ......................................................................................
30
Table 8 - Predisposing Factors for Exertional Heat Stroke ..................................
31
C3.1.9.3. Diagnosis of Heat Stroke................................................................................... 31
Table 9 - Symptoms, Signs, and Findings in Heat Stroke .................................... 33
C3.1.9.4. Criteria for Making the Diagnosis of Heat Stroke ............................................ 33
C3.1.10. Severe Exertional Heat Injury (“Exertional Heat Illness”) .................................... 34
CHAPTER 4:............................................................................................................................... 35
C4. TREATMENT OF HEAT STROKE ................................................................................. 35
C4.1. Treatment of Heat Stroke - General ................................................................................ 35
C4.1.1. Cooling..................................................................................................................... 35
C4.1.1.1.1. Clothing Removal ...................................................................................... 35
C4.1.1.1.2. Fanning....................................................................................................... 35
C4.1.1.1.3. Cold or Ice Water Immersion..................................................................... 35
C4.1.1.1.4. Cold Packs, Cooling Blankets, Fanning, Mists, Cooling Units ................. 36
C4.1.2. Cardiovascular Support............................................................................................ 36
C4.1.3. Concomitant Therapy............................................................................................... 37
C4.2. Treatment of Heat Stroke - Clinical ................................................................................
37
C4.2.1. Preliminary Studies and Procedures......................................................................... 37
C4.2.1.1.1. Shivering ....................................................................................................
38
C4.2.1.1.2. Electrolyte Abnormalities ..........................................................................
38
C4.2.1.1.3. Rhabdomyolysis......................................................................................... 38
C4.2.1.1.4. Renal Injury................................................................................................ 39
C4.2.1.1.5. Other Associated Injury ............................................................................. 39
CHAPTER 5:............................................................................................................................... 40
C5. FOLLOW-UP OF HEAT STRESS INJURIES.................................................................
40
C5.1. Monitoring Health after Heat Stroke Recovery ..............................................................
40
C5.2. Care of Residual Disability or Deficits after Heat Stroke...............................................
40
C5.3. Re-Exposure to Heat .......................................................................................................
40
C5.3.1. Minor Injuries........................................................................................................... 40
C5.3.2. Major Injuries...........................................................................................................
40
C5.3.2.1.1. Heat Exhaustion .........................................................................................
40
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
iv
C5.3.2.1.2. Heat Stroke................................................................................................. 41
C5.4. Reporting......................................................................................................................... 41
C5.5. Prevention of Further Heat Stress Injuries in the Population.......................................... 41
CHAPTER 6:...............................................................................................................................
42
C6. CRITERIA FOR THE DIAGNOSIS OF HEAT STROKE.............................................
42
Table 10 - Diagnostic Criteria for Heat Stroke..................................................... 43
CHAPTER 7:............................................................................................................................... 44
C7. PHYSIOLOGY OF COLD STRESS ................................................................................. 44
C7.1. Introduction .....................................................................................................................
44
C7.1.1. Heat Transfer or Loss from the Human Body..........................................................
44
C7.1.2. Cold Stress, Cold Strain, and Cold Injury................................................................ 44
C7.2. Environmental Cold Stress Factors................................................................................. 44
C7.2.1. Temperature and Wind............................................................................................. 44
C7.2.2. Windchill Temperature Index .................................................................................. 45
C7.2.3. Humidity and Moisture ............................................................................................ 45
C7.2.4. Immersion................................................................................................................. 45
C7.2.4.1. Diving Reflex .................................................................................................... 45
C7.2.4.2. Fluid shifts in Cold Water ................................................................................. 46
C7.2.4.3. Performance in Cold Water............................................................................... 46
C7.2.4.4. Swimming Induced Pulmonary Edema (SIPE)................................................. 46
C7.2.4.5. Awareness of Cold Strain in Cold Water.......................................................... 46
C7.2.4.6. Cardiac Output in Cold Water........................................................................... 46
C7.2.4.7. Survival Times in Cold Water........................................................................... 46
Figure 6 - Survival Time in Cold Water (estimated) ............................................ 47
C7.2.4.8. Diving Suits....................................................................................................... 47
C7.2.5. Elevation (Altitude).................................................................................................. 48
C7.2.6. Contact and Handling of Cold Objects .................................................................... 48
C7.2.6.1. Time to Reach Contact Temperature ................................................................ 48
C7.2.6.2. Dexterity when Handling Cold Objects ............................................................
49
C7.2.6.3. Freezing to Cold Objects................................................................................... 49
C7.2.7. Ultraviolet Light....................................................................................................... 49
C7.3. Individual Cold Stress Factors ........................................................................................
49
C7.3.1. Body Mass and Fat...................................................................................................
49
C7.3.2. Gender ...................................................................................................................... 49
C7.3.3. Age ........................................................................................................................... 49
C7.3.4. Race and/or Ancestral Geographic Location ........................................................... 50
C7.3.4.1. Metabolic Adaptation........................................................................................
50
C7.3.4.2. Insulative Adaptation ........................................................................................ 50
C7.3.4.3. Hypothermic Adaptation...................................................................................
50
C7.3.5. Alcohol.....................................................................................................................
50
C7.3.6. Hydration..................................................................................................................
50
C7.3.7. Central Nervous System (CNS) Abnormalities ....................................................... 51
C7.3.8. Heat Debt..................................................................................................................
51
C7.4. Compensation for Cold Environments............................................................................
51
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
v
C7.4.1. Functioning in Cold Environments .......................................................................... 51
C7.4.2. Metabolism............................................................................................................... 52
C7.4.2.1. Muscles.............................................................................................................. 52
C7.4.2.2. Body Fat ............................................................................................................
52
C7.4.2.3. Hormones ..........................................................................................................
52
C7.4.2.4. Calories and Cold Exposure.............................................................................. 52
C7.4.2.4.1. Caloric requirements .................................................................................. 52
C7.4.2.4.2. Appetite ...................................................................................................... 53
C7.4.3. Cardiovascular..........................................................................................................
53
C7.4.3.1. Shunting ............................................................................................................
53
C7.4.3.2. Blood Pressure................................................................................................... 53
C7.4.3.3. Heart Rate and Cardiac Output ......................................................................... 53
C7.4.3.4. Oxygen Consumption........................................................................................ 53
C7.4.4. Respiratory Tract and Ventilation Changes .............................................................
53
C7.4.5. Shivering ..................................................................................................................
54
C7.4.5.1. Metabolism of Shivering................................................................................... 54
C7.4.5.2. Peak Shivering Metabolic Rate Equation.......................................................... 54
C7.4.6. Fatigue...................................................................................................................... 54
C7.4.7. Circadian Rhythm (Body Clock).............................................................................. 54
C7.5. Acclimatization ............................................................................................................... 55
C7.5.1. Acclimatization and Acclimation............................................................................. 55
C7.5.2. Effects of Acclimatization........................................................................................ 55
C7.5.3. Limitations of Acclimatization................................................................................. 56
C7.5.4. Development of Acclimatization ............................................................................. 56
C7.5.4.1. Altitude.............................................................................................................. 56
C7.5.4.2. Local (Rather than Whole Body) Acclimatization............................................ 56
C7.5.5. Habituation............................................................................................................... 56
C7.5.6. Non-Shivering Thermogenesis................................................................................. 57
CHAPTER 8:............................................................................................................................... 58
C8. PREVENTION OF COLD STRESS INJURIES ..............................................................
58
C8.1. Measurement of Cold Stress Effects on the Body........................................................... 58
C8.1.1. Core Body Temperature ...........................................................................................
58
C8.1.2. Skin or Local Temperature.......................................................................................
58
C8.1.3. Cold Strain Index ..................................................................................................... 58
C8.2. Identifying Risk Factors.................................................................................................. 58
C8.2.1. Protective Clothing................................................................................................... 58
C8.2.2. Ointments, Lotions, Creams, Emollients, etc...........................................................
58
C8.2.3. Vasospastic Syndrome ............................................................................................. 59
C8.2.4. Motion Sickness .......................................................................................................
59
C8.2.5. Shapiro’s Syndrome ................................................................................................. 59
CHAPTER 9:............................................................................................................................... 60
C9. DIAGNOSIS AND TREATMENT OF COLD STRESS INJURIES..............................
60
C9.1. Dermatological (Skin) injuries........................................................................................ 60
C9.1.1. Conditions Unmasked or Exacerbated by Cold Exposure .......................................
60
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
vi
C9.1.1.1. Acrocyanosis ..................................................................................................... 60
C9.1.1.2. Rosacea.............................................................................................................. 60
C9.1.1.3. Cold Agglutinin Disease ................................................................................... 60
C9.1.1.4. Cold Panniculitis ...............................................................................................
60
C9.1.1.5. Xerosis...............................................................................................................
60
C9.1.1.6. Cold-induced Urticaria...................................................................................... 60
C9.1.2. Chilblain................................................................................................................... 61
C9.2. Injuries of the Extremities Due to Cold Exposure .......................................................... 61
C9.2.1. Frostbite....................................................................................................................
61
C9.2.1.1. Mechanisms (Pathophysiology) of Frostbite.....................................................
61
C9.2.1.1.1. Hunting reaction......................................................................................... 62
Figure 7 - Pathophysiology of Frostbite ............................................................... 62
C9.2.1.2. Frostbite Risk Factors........................................................................................ 62
C9.2.1.3. Classification of Frostbite .................................................................................
63
C9.2.1.3.1. Frostnip.......................................................................................................
63
C9.2.1.3.2. First Degree Frostbite................................................................................. 63
C9.2.1.3.3. Second Degree Frostbite ............................................................................ 64
C9.2.1.3.4. Third Degree Frostbite ............................................................................... 64
C9.2.1.3.5. Fourth Degree Frostbite ............................................................................. 64
C9.2.1.4. Evaluation.......................................................................................................... 64
C9.2.1.5. Treatment of Frostbite....................................................................................... 65
C9.2.1.5.1. Rewarming ................................................................................................. 65
C9.2.1.5.2. Rest............................................................................................................. 65
C9.2.1.5.3. Blood Flow................................................................................................. 65
C9.2.1.5.4. Neurological ............................................................................................... 66
C9.2.1.5.5. Hyperbaric Oxygen .................................................................................... 66
C9.2.1.5.6. Surgery ....................................................................................................... 66
C9.2.1.5.7. Prevention of Infection............................................................................... 66
C9.2.1.5.8. Recovery..................................................................................................... 66
Table 11 - Frostbite Rewarming Protocol............................................................. 67
C9.2.2. Trench Foot (Trenchfoot).........................................................................................
67
C9.2.2.1.1. Stages of Trench Foot ................................................................................ 68
C9.2.2.1.2. Treatment of Trench Foot ..........................................................................
68
C9.2.2.1.3. Disposition .................................................................................................
69
C9.2.3. Vibration White Finger ............................................................................................ 69
C9.2.4. Raynaud’s Phenomenon........................................................................................... 69
C9.2.5. Cold Agglutinin Disease ..........................................................................................
69
C9.2.6. Paroxysmal Cold Hemoglobinuria........................................................................... 69
C9.3. Ocular (Eye) injuries Due to Cold Exposure ..................................................................
70
C9.3.1. Snow Blindness (Acute Photokeratitis, Solar Keratitis) .......................................... 70
C9.3.2. Cold Keratopathy (Corneal Epithelial Cold injury) ................................................. 70
Figure 8 - Corneal Staining in Cold Keratopathy .................................................
70
C9.3.3. Corneal Frostbite ...................................................................................................... 71
C9.4. Hypothermia....................................................................................................................
71
C9.4.1. Public Health Impact of Hypothermia .....................................................................
71
C9.4.2. Symptoms and Signs of Hypothermia......................................................................
72
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
vii
C9.4.3. Classification of Hypothermia ................................................................................. 72
Table 12 - Classification of Hypothermia............................................................. 72
C9.4.4. Survival of Hypothermia.......................................................................................... 73
Table 13 - Hypothermia Survival Factors.............................................................
73
Table 14 - Physiologic Changes During Hypothermia.........................................
74
C9.4.5. Predisposing Factors for Hypothermia..................................................................... 74
Table 15 - Predisposing Factors in Hypothermia ................................................. 74
C9.4.5.1. Ethanol and Medications................................................................................... 75
C9.4.5.2. Clothing.............................................................................................................
75
C9.4.6. Treatment of Hypothermia.......................................................................................
75
C9.4.6.1. Rewarming Methods ......................................................................................... 76
C9.4.6.2. Afterdrop ........................................................................................................... 76
C9.4.6.3. Extreme Cases of Hypothermia......................................................................... 76
C9.4.6.3.1. Cardiopulmonary Bypass ...........................................................................
76
C9.4.6.3.2. Bretylium....................................................................................................
77
Figure 9 - Hypothermia Treatment Algorithm...................................................... 78
C9.4.6.3.3. Triage ......................................................................................................... 78
C9.4.6.3.4. Potential Complications ............................................................................. 79
C9.4.7. Follow-up of Hypothermia....................................................................................... 79
C9.4.8. Prognosis in Hypothermia........................................................................................ 79
C9.4.8.1. Predicting Outcome in Hypothermia................................................................. 79
C9.4.8.2. Elderly Victims ................................................................................................. 79
C9.4.8.3. Pediatric Victims............................................................................................... 79
Figure 10 - Assessment (Category) of Cold Injury............................................... 80
C9.5. Prevention of Further Heat Stress injuries in the Population.......................................... 80
CHAPTER 10:............................................................................................................................. 81
C10. REPORTING ..................................................................................................................... 81
CHAPTER 11:............................................................................................................................. 82
C11. HEAT STRESS INJURIES PREVENTION AND TREATMENT...............................
82
C11.1. Prevention of Heat injuries............................................................................................ 82
C11.1.1. Minor Heat Injuries ................................................................................................ 83
C11.1.1.1. Miliaria............................................................................................................
83
C11.1.1.2. Heat Syncope...................................................................................................
83
C11.1.1.3. Heat Edema ..................................................................................................... 83
C11.1.1.4. Heat Tetany ..................................................................................................... 83
C11.1.1.5. Heat Cramps.................................................................................................... 83
C11.1.2. Major Heat Injuries ................................................................................................
83
C11.1.2.1. Heat Exhaustion .............................................................................................. 83
C11.1.2.2. Heat Stroke......................................................................................................
84
C11.2. Cooling.......................................................................................................................... 84
C11.3. Reporting Heat injuries ................................................................................................. 84
CHAPTER 12:.............................................................................................................................
85
C12. COLD STRESS INJURIES PREVENTION AND TREATMENT .............................. 85
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
viii
CHAPTER 13:............................................................................................................................. 87
C13. REFERENCES................................................................................................................... 87
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
1
Chapter 1:
C1. Introduction
This technical manual serves to contain current Navy knowledge on heat and cold stress
injuries, including their causes, prevention, treatment, and effects. It seeks to document what is
scientifically sound and generally accepted medical information. Experimental procedures and
potential avenues of research are avoided, although possible treatments and protocols may be
mentioned in some instances. The target audience for this document is the Navy medicine
community, specifically corpsmen, nurse practitioners, and physicians caring for personnel
potentially suffering from the effects of heat or cold stress exposure. Hyperlinks are included as a
tool for physicians and others with further interest in the subject matter. This document is not
meant as a replacement for the Manual of Naval Preventive Medicine NAVMED P-5010, but
rather may be considered a supplement or foundational technical manual on heat and cold stress
injuries. With the publication of this revised technical manual, all previous Navy documents
dealing with the prevention and treatment of heat and cold stress injuries will be obsolete and
replaced by this document and the P-5010.
Heat and cold stress can significantly affect military readiness and performance, and
historically have had major impact on military campaigns. Leaders who push personnel in the
presence of heat or cold stress exposure risk disaster. Outdated, erroneous thinking about
developing “dehydration tolerance” or that one’s unit can “stand” more than another because
they are “tougher” or “more motivated” must be replaced by leadership decisions based on
proven facts about heat and cold stress exposure. To that end, this manual is a ready repository of
information for the supervisor or commander. All supervisors should be familiar with the
documents in C11. Heat Stress Injuries Prevention and Treatment and C12. Cold Stress Injuries
Prevention and Treatment which briefly summarize relevant information for those not involved
with patient care. The main document text gives further details.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
2
Chapter 2:
C2. Physiology of heat stress
C2.1. Heat Transfer and the Human Body
Heat is transferred to and from the human body by four mechanisms: convection,
conduction, radiation, and evaporation (which is actually a form of convection). Convection is
the transfer of heat from the source by heating the surrounding medium, which is then moved to
the body (such as heated air moved by a ventilation system fan) to a living area. Conduction is
the transfer of heat from the source through an object or liquid that is warmed first. An example
is an electric coil heating a chair that in turn heats the person sitting in the chair. Radiation is the
transfer of heat from the source without warming the intervening space. Examples include heat
from the sun warming the earth, and heat from a radiator warming a person. Evaporation causes
the removal of heat from an object by the vaporization of liquid, as when a person cools by
sweating.
C2.1.1. Heat Equation
The net amount of heat in the human body is represented by the Heat Equation (also
called the "Heat Balance Equation") [PMID 1180844],
1
as follows.
Heat production (measured by the metabolic rate)
+ radiant heat gain or loss
+ convective heat gain or loss
+ conductive heat gain or loss
– evaporative cooling
= heat storage (in man)
This may be represented by the formula: M + R + C - E = S
C2.1.2. Heat Dissipation (Removal)
The body constantly loses heat through breathing and convection (air moving over
exposed skin, especially the head and neck). Minor amounts of heat are also lost through
urinating and defecating. In heat stress conditions, the body’s primary mechanism of excess heat
removal is sweating (the loss of perspiration through the skin).
C2.1.2.1. Sweating (Perspiration)
Sweating is the main mechanism the body uses to remove heat from itself in hot weather.
The evaporation of sweat can cool the body even when surrounding temperatures are greater than
body temperature.
Sweat gland function increases when skin (not air) temperature approaches 95° F (35° C)
[CHIPPM].
2
Sweating depends on sufficient hydration, adequate blood flow to the skin, and
proper operation of sweat glands, which are under neurologic [PMID 1442139]
3
and hormonal
control (including growth hormone [PMID 11474638],
4
[PMID 11106921],
5
sex hormones
[PMID 1947733],
6
and prolactin [PMID 3780532]
7
[PMID 3397041],
8
and subject to
pharmacologic influence, such as cholinergics or anticholinergics [
PMID 2120621].)
9
Women
tend to sweat less profusely than men [
PMID 10414066]
10
[PMID 8504843].
11
Sweating
efficiency is not influenced by exercise intensity [
PMID 8851527].
12
Sweating efficiency in
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
3
removing body heat is influenced by environmental factors, especially humidity (reflecting the
partial pressure of water in the atmosphere) and wind speed.
Theoretically, water can remove up to 540 calories (kcal) per liter (heat of vaporization of
water = 540 calories/gram = 0.54 kcal/g = 2260 joules/g). However, sweating is less efficient at
cooling than that. Not all sweat evaporates, especially at high rates of sweating (or low rates of
evaporation, as in high humidity), when sweat may run or drip off the body or be absorbed by
clothing [PMID 1193094].
13
C2.1.2.1.1. Skin Heat, Moisture, and Texture
A normal response to heat stress exposure is increased cutaneous blood flow and
increased sweating [PMID 481154].
14
Hot moist skin is expected in individuals perspiring
normally in heat stress conditions. If there is lack or cessation of sweating (anhydrosis), heat
buildup (“heat storage”) will occur. If heat buildup continues, body temperature will become
high enough to cause injury and, eventually, death. Hot dry skin may be found in conditions of
heat stress when the ability to perspire has been compromised. This signals dangerous
accumulation of body heat.
Cool dry skin is abnormal in the presence of heat stress, and may signal blood shunting
away from the skin and the cessation of sweating. Cool moist (“clammy”) skin may signal that
blood shunting away from the skin has occurred, with moisture on the skin remaining from
previous sweat that has not evaporated due to a humid atmosphere.
C2.1.2.1.2. Blood Shunting
Blood shunting refers to diminished cutaneous blood flow, resulting in diminished ability
to lose heat from the skin. During heat stress, skin blood flow can be 60% of cardiac output
[PMID 8504843].
15
In heat stress conditions, blood flow to the skin must be maintained so that
heat loss (especially by evaporation through sweating) can occur. However, during exercise,
blood flow to muscles dramatically increases. For example, calf blood flow rises 20-fold with
exercise [PMID 10747200].
16
Vigorous exercise appears to limit cutaneous blood flow [PMID
591471].
17
If cutaneous blood flow is limited by shunting away from the skin (as may also
happen in severe heat injuries), heat loss diminishes and body core temperature may rise to
hazardous levels.
In addition to blood shunting from cutaneous circulation, as body temperature rises,
blood flow through splanchnic circulation initially decreases significantly (enabling maintenance
of blood pressure). As temperature continues to increase, however, splanchnic circulation
suddenly is re-established, possibly signaling loss of that compensatory mechanism [
PMID
3403442].
18
C2.1.2.1.2.1. Thirst
Thirst is a mechanism the body uses to signal the need for water replacement. In
sedentary non-heat stress conditions, drinking to quench thirst adequately regulates body
hydration. However, in exercise heat stress conditions, thirst sensation lags behind the actual
need for water. Spontaneous drinking does not start until >2% of body weight is lost [PMID
10036337].
19
If a person only drinks to quench his or her thirst, water intake will lag behind
water loss for up to several hours after heat stress conditions cease. Thus, thirst should not be the
only drive for water when personnel are active in heat stress conditions. Instead, personnel
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
4
should be instructed on the need to drink water replacement beyond what thirst dictates, and
should be encouraged to drink while in heat stress conditions.
C2.1.2.1.2.2. Drinks
C2.1.2.1.2.2.1. Water
To make water freely available to workers is essential; to encourage water drinking in
heat stress conditions is important, as thirst can lag behind water deficit by several hours.
Water is an ideal rehydration drink. It is absorbed rapidly from the upper gastrointestinal
(GI) tract, and it is generally inexpensive and readily available. However, many people find plain
water less palatable than flavored drinks. Palatability of drinks is important in stimulating intake
and ensuring adequate volume replacement [
PMID 9298549].
20
In severe heat stress conditions
over a prolonged period (e.g., working 5 days in the desert), water alone appeared to provide
adequate hydration when compared to carbohydrate-electrolyte beverages, with or without a
small amount of glycerol [PMID 8588794].
21
C2.1.2.1.2.2.2. Sports Drinks
Sports drinks (Gatorade®, Powerade®, etc.), sometimes referred to as “carbohydrate-
electrolyte (CHO-E) fluid replacement,” are generally sweetened, flavored drinks that contain
some or all of the electrolytes lost in sweat. They are absorbed at approximately the same rate as
water, and cost more. Sports drinks are acceptable fluid replacement beverages in heat stress
conditions. However, that they are superior to water is not universally accepted; also, the need to
use them to replace electrolytes is not established in conditions where a normal diet is consumed,
workers are heat-acclimatized (as people are acclimatized, they lose less salt in their sweat), and
there is not prolonged heat stress or time between eating or an unusual performance requirement.
Sports drinks do have the advantage that, to some people, they taste better than water and thus
are more likely to be consumed by those that do not like drinking pure water (and thus may be
more likely to maintain better hydration). Sports drinks also contain sugar, which may be
advantageous in special nutrition or performance situations. In one study, CHO-E increased the
frequency of task completion, elevated blood glucose, and reduced perceived exertion, but
provided no additional benefits with regard to hydration status and physiological function during
loaded walking under heat stress [
PMID 16173217].
22
Potential caloric intake from sports drinks can be substantial. Five quarts of 5.8%
carbohydrate solution (e.g., Gatorade®)
23
would provide 1,120 kilocalories, and five quarts of
8% carbohydrate solution would provide 1,545 kilocalories; for this reason, sports drinks
generally should not be used to totally replace water consumption.
The following criteria for sports drinks have been suggested by the U.S. Army: sodium
15 to 30 milimole (mmol)/L, potassium 2 to 5 mmol/L, and carbohydrate 5% to 10%; high
fructose should be avoided as it may cause gastrointestinal side effects [CHIPPM].
24
Water is the preferred employer-provided hydration beverage unless workers will be
expected to work long hours between meals (6 hours or more) or have unusual performance
requirements (e.g., heavy labor in enclosing PPE such as chemical protective suits, certain
special operations). Individuals with medical conditions affecting performance or health in heat
stress conditions may also benefit from sports drinks as opposed to water; however, such
decisions are the responsibility of the health care provider.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
5
C2.1.2.1.2.2.3. Oral Rehydration Salts (ORS)
ORS, when mixed with the prescribed quantity of water, may also be used as a
rehydration liquid. However, ORS were developed as fluid replacement for GI loss and may
have more salt (sodium) than is necessary. For example, ORS has about 2 grams (90 mmol) of
sodium per liter [WHO],
25
while Gatorade® has less than 0.5 grams of sodium per liter [Stokely-
Van Camp].
26
C2.1.2.1.2.2.4. Carbonated Beverages
Carbonated beverages (sodas) are prone to be acidic, cause belching, may take longer to
absorb because of their high sugar content, may cause a full feeling and reduce consumption, and
may be more expensive than water or sports drinks. However, because many people prefer
carbonated beverages to water or sports drinks, carbonated drinks may be acceptable rehydration
beverages (i.e., water is better than soda, but soda is better than nothing). For most people,
carbonated beverages are not recommended as a water substitute.
C2.1.2.1.2.2.5. Alcoholic Beverages
Alcoholic beverages may cause abnormal GI absorption, vasodilation, sweating, impaired
judgment, and increased urination. Thus, they may be dangerous in heat stress situations and are
unacceptable as rehydration beverages.
C2.1.2.1.2.3. Intravenous Rehydration
Using intravenous (IV) fluids to replace fluids in heat stress conditions when no injury
exists is unnecessary for healthy persons. Although plasma volume may be replaced more
rapidly, research has not found IV rehydration advantageous over oral rehydration in regards to
physiological strain, heat tolerance, or thermal sensations [PMID 17146319].
27
C2.1.2.1.2.4. Water Absorption
Food can delay gastric emptying and GI absorption of water. Hypotonic fluids (plain
water or dilute solutions of carbohydrates) are emptied from the stomach more rapidly than
fluids with higher concentrations of carbohydrates [PMID 2733575].
28
High concentrations of
sugar, complex carbohydrates, proteins, and, especially, fats, all may hinder water absorption,
and thus are undesirable in water-replacement beverages. However, ingestion of carbohydrate-
electrolyte drinks in the post-exercise period restores exercise capacity more effectively than
plain water [
PMID 9298549].
29
With increasing glucose concentration, the rate of fluid delivery
to the small intestine is decreased, but the rate of glucose delivery is increased [PMID
1895359,
30
PMID 2733575].
31
Mild exercise increases gastric emptying, while maximal exercise
delays gastric emptying [PMID 1928033].
32
C2.1.2.1.3. Sodium (Salt)
Sodium (in salt) is lost through sweating. Salt tablets or salt supplements are not
recommended. Normal military dietary intake is adequate to supply sufficient replacement
sodium, except possibly during the first few days of heat exposure [
PMID 10919961].
33
Under
certain extreme conditions, especially with protracted heat stress exposure and limited dietary
sodium, supplemental salt may be required. However, medical consultation should be obtained
before salt supplements are used.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
6
C2.2. Environmental Heat Stress Factors
C2.2.1. Measurement of Temperature
The obvious and most environmental heat stress factor is temperature. The single best
measure of environmental heat stress is the Wet Bulb Globe Temperature (WBGT) Index. The
WBGT takes into account several factors, including temperature, radiant heat (sun), humidity,
and air flow. It is calculated as follows.
WBGT = (Wet Bulb x 0.7) + (Globe Temperature x 0.2) + (Dry Bulb x 0.1)
Thus, Wet Bulb (a thermometer covered by a wet cloth or wick, to account for
evaporative cooling) accounts for 70% of the WBGT. (By Navy convention, evaporation in mild
airflow is considered more representative of actual work conditions; hence the name “aspirated”
wet bulb.) Globe Temperature (a thermometer enclosed in a black globe in the sun) accounts for
20% of the WBGT. Dry Bulb (a dry thermometer in the shade) accounts for 10% of the WBGT.
Currently, rather than calculate the WBGT from three separate instruments, the Navy
uses the Wet-Bulb Globe Temperature Meter, also known as the Heat Stress Meter, to measure
the WBGT. The instrument displays each of these values as well as computes and displays the
WBGT Index value. The approved Navy Heat Stress Meter is part number 70-6685-01-055-
5298.
C2.2.2. Wind
Wind has a cooling effect that increases with air velocity. Under certain conditions, at
approximately 1,500 feet per minute (17 miles per hour), friction begins to generate enough heat
that the rate of cooling begins to decline; also, when air temperature exceeds 95° F (35° C), air
velocities greater than 300 feet per minute (3.4 miles per hour) may be undesirable [NEHC-
TM92-6].
34
However, in some conditions workers have requested supplemental intermittent
cooling air at velocities as high as 3,000 feet per minute (34 miles per hour) [Jorgensen].
35
C2.2.3. Humidity.
High humidity decreases the rate of water evaporation at a given temperature. Since
sweating removes body heat by evaporative cooling, conditions of high humidity increase heat
stress because sweating becomes less effective at cooling the body. Thus, strenuous exercise at
85° in 90% humidity (for example, in a temperate climate coastal area) may be more heat
stressful than at 100° in 10% humidity (for example, in a equatorial desert area).
C2.2.3.1. Heat Index
The “heat index” is a calculation that takes the relative humidity and the environmental
temperature into account to estimate how hot conditions “feel” to people. According to the
National Weather Service,
36
a currently used heat index equation is as follows.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
7
Figure 1- Heat Index Equation
Heat Index =
- 42.379
+ 2.04901523T
+ 10.1433127R
- 0.22475541TR
- 6.83783x10
-3
T
2
- 5.481717x10
-2
R
2
+ 1.22874x10
-3
T
2
R
+ 8.5282x10
-4
TR
2
- 1.99x10
-6
T
2
R
2
where T = ambient dry bulb temperature (in degrees Fahrenheit between 80 and 110)
and R = relative humidity between 10 and 90 percent.
The Heat Index is an APPARENT TEMPERATURE, and may not be valid for calculated
values above 135° F. Heat index tables and calculators are available on the Internet. A heat index
calculator is also available here for those using Microsoft Internet Explorer®. It is important to
note that the “heat index” is not a complete measure of heat stress conditions, and THE HEAT
INDEX IS NOT TO BE SUBSTITUTED FOR THE WBGT INDEX IN CALCULATING
HEAT STRESS OR STAY TIMES.
C2.2.3.1.1. Physiologically Equivalent Temperature
The Physiologically Equivalent Temperature (PET) is a term referring to the indoor air
temperature at which body core temperature and skin temperature is the same as in given
conditions outdoors. It is based on a European model of heat balance (the Munich Energy
balance Model for Individuals), and seeks to present a model of human body heating and cooling
indoors that is equivalent to what would be experienced outdoors. For example, on hot summer
days with direct solar irradiation, the PET value may be more than 36° F higher than the air
temperature, on a windy day in winter up to 27° F lower [
PMID 10552310].
37
C2.2.4. Rain
Rain is generally accompanied by overcast skies (decreasing direct sunlight), and
raindrops are generally cooler than body temperature (and thus cool by conductive heat loss).
However, rain is usually present with high humidity (decreasing evaporative cooling), and
significant heat stress conditions may exist even when it is raining.
C2.2.5. Sun Position and Time of Day
The higher the
position of the sun in the sky, the more radiant heat will be absorbed from
surrounding terrain and from the sun. Shade afforded by trees or buildings may not only block
sunlight, but on windless days may also afford relief from convective heat (hot air currents). In
the winter, the sun is nearer the horizon, decreasing radiant heat absorption. (It is to be cautioned
that winter sun can still present a sunburn hazard.)
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
8
C2.2.6. Elevation
While temperatures are decreased with increased elevation, the health risk from heat
stress is increased in deep mines. The incidence rate ratio of heat exhaustion for Australian mines
operating below 1,200 meters compared with those operating above 1,200 meters was 3.17
[PMID 10810098].
38
Indoor sources of heat such as furnaces, radiators, recently cast or rolled
metal (for example, rolls of sheet steel) may add significant radiant heat stress to personnel.
C2.3. Individual Heat Stress Factors
C2.3.1. Sunburn
Sunburn (a result of over exposure to the sun, not discussed here) can decrease sweating,
and thus may impair heat loss and the body’s ability to tolerate heat stress (although elevated
core temperature was not found in an experimental study) [PMID 1566925].
39
C2.3.2. Clothing and Personal Protective Equipment (PPE)
Since heat loss through sweating depends on evaporation, clothing or gear that decreases
skin exposure may increase heat stress. Long sleeves and pants may decrease heat stress from
radiant solar heat more than short sleeves and shorts, even though wearing long clothing may
feel less comfortable [PMID 10901990]. In conditions of high humidity, the heat stress added by
protective clothing may be especially significant. Heat strain indices, including tolerance time,
are significantly affected by extremes of humidity during both light and heavy exercise while
wearing a semi-permeable nuclear, biological and chemical protective clothing ensemble [PMID
8971493].
40
The American Conference of Governmental Industrial Hygienists (ACGIH) has
suggested that WBGT values should be increased by 6.3° F (3.5° C) when cloth coveralls are
worn, and 9° F (5° C) when double-cloth coveralls are worn (impermeable, water vapor resistant,
and encapsulating suits excluded) (see Table 5) [ACGIH].
41
Respirator use while working in heat stress significantly increases respiratory rate, heart
rate, and, at high levels of work, systolic blood pressure. Air temperatures immediately anterior
to the face of respirator wearers have been found to increase an average of 13.5° F (7.5° C).
Also, as work intensity of respirator wearers increases, so does breathing resistance [PMID
1858664].
42
C2.3.3. Illness
Underlying illness (infections, hypertension, diabetes, sickle cell trait [PMID 8677839],
43
congestive heart failure [PMID 16216975],
44
etc.) may impair the ability of the body to tolerate
heat stress. Exposure to hot environmental conditions is not recommended for diabetic patients,
although research-based support for such a recommendation, while not absent, is not robust at
this time [PMID 7698855].
45
Any condition associated with diarrhea, vomiting, polyuria,
impaired thirst or sweating, or altered consciousness may decrease heat stress tolerance.
Disabilities may hinder individuals from normal responses to heat stress (such as moving
out of the sun or away from other heat sources, getting to or drinking sufficient water, etc.), or
may force persons to perform certain actions in such a way that more heat is generated than
would be generated by persons without the disability.
C2.3.4. Immunizations (Vaccinations, Inoculations)
Immunizations in progress (i.e., recent immunizations) may place additional stress on the
body, possibly resulting in diminished heat stress tolerance [PMID 10050577].
46
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
9
C2.3.5. Prior Heat Stress Injury
A past medical history that includes heat illness or injury may limit tolerance to heat
stress conditions. Such individuals may require additional time for acclimatization, and may
never be able to tolerate heat stress as well as persons who have not sustained heat stress-related
injury [PMID 2406545].
47
C2.3.6. Recent Heat Stress Exposure
In addition to a history of prior heat stress injury, recent exposure to heat stress
conditions (e.g., the previous day) has been associated with increased risk of exertional heat
illness in two studies of U.S. Marine Corps recruits [
PMID 8900989,
48
PMID 15632673].
49
Similarly, competition over several days in heat stress conditions has been associated with heat
cramps in athletes [
PMID 8653105].
50
Whether this is limited to exercise in heat stress
conditions only subsequent to some degree of tissue injury is suspected by researchers
(Sawka),
51
but is not yet established in the medical literature.
C2.3.7. Size
Larger individuals generate more heat than others (simply because they have more body
tissue undergoing metabolism). Additionally, the volume to surface area ratio is higher in large
individuals. Thus, there is relatively less surface area (skin) through which to lose heat. The
percentage of fat and the surface to mass ratio were found to have the largest effect in one
investigation of the relative influence of fitness, acclimatization, gender and anthropometric
measures on the physiological responses to heat stress [PMID 2079061].
52
Body mass index (BMI), also called Quetelet’s index and used to evaluate obesity [PMID
4030199],
53
is used in calculations of heat stress. The BMI is calculated using body height and
weight (mass). The BMI equation is BMI = weight in pounds ÷ (height in inches)
2
x 703. The
metric system formula is BMI = weight in kilograms ÷ (height in meters)
2
. Units will be kg / M
2
[CDC].
54
The CDC also has a BMI calculator available on the Web [CDC].
55
C2.3.8. Population Characteristics
In civilian populations, there is an increased prevalence of heat injury risk factors,
including older age, medication use (especially anticholinergic and psychotropic medications),
obesity, previous heat injury, skin disorders [
PMID 9002705],
56
and persons in whom is a
greater number of chronic medical illnesses [PMID 11434495].
57
C2.3.9. Gender
Male and female body mass index values are different, due to the relative size
differences. Water content varies slightly between males and females. Approximately 60% of an
average 70 kg man’s body weight is water. Of the 42 liters of water, 28 L is in intracellular fluid
and 14 L in extracellular (mostly interstitial) fluid; female water content is somewhat lower
because of the higher adipose tissue to lean body mass ratio [PMID 10036337].
58
This difference
of water and fat content may be the reason that females have been found by some studies to be at
a thermoregulatory disadvantage compared with males when wearing protective clothing and
exercising in a hot environment [PMID 9660153].
59
(However, not all studies are in agreement
with that finding [
PMID 655995].)
60
A U.S. Army study (“the largest and most comprehensive
epidemiological study of exertional heat injury”) found that women are at increased risk of heat
stroke [PMID 16118581].
61
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
10
Core body temperature of females may increase (approximately 0.5 degrees) during the
menstrual cycle. However, this temperature elevation has not been found to be significant in
tolerating heat stress during exercise [PMID 750842],
62
[PMID 7181811].
63
One study of females
in the Canadian military found that exertional heat tolerance was increased during the early
follicular phase in women who did not use oral contraceptives [PMID 10408316].
64
One
reviewer has concluded that “aerobic capacity, surface area-to-mass ratio, and state of
acclimation are more important than sex in determining physiological responses to heat stress”
[PMID 3888617].
65
Pregnant individuals become less tolerant of heat stress as pregnancy continues. In
addition to being a source of metabolic heat and increased weight to the mother, the unborn child
may also be susceptible to heat injury [PMID 6446171].
66, 67
C2.3.10. Age
Young children and the elderly have decreased toleration of heat stress. For morphologic
and physiologic reasons, exercising children do not adapt as effectively as adults when exposed
to high climatic heat stress [PMID 10878169].
68
Aging is associated with decreased heat
tolerance [PMID 3324259].
69
Whether this is due to age-related cardiovascular factors [PMID
3749652]
70
or other factors is uncertain [PMID 3324259].
71
In older men, rectal temperature
increases more rapidly and to greater magnitude, osmolality restoration after rehydration is
slower, and thirst is less, while average total body sweat rates and chest sweat rates were not
significantly different than in younger men [PMID 2589532].
72
C2.3.11. Race
Dark-colored clothing absorbs heat more readily than light-colored clothing [PMID
4068337].
73
However, the difference in heat tolerance in the sun by individuals of different skin
colors has not been found to be significant [PMID 6736576].
74
C2.3.12. Acclimatization
Acclimatization is the process of physiologic adaptation to heat stress conditions. (Note:
some sources equate this to “acclimation” [Stedman’s],
75
whereas others distinguish between
“acclimation,” or short-term adaptation in laboratory conditions, and “acclimatization,” or
longer-term adaptation to heat in field conditions [
PMID 11252069].)
76
After acclimatization,
tolerance of and performance in heat stress conditions is improved. When the body is repeatedly
exposed to heat stress, sweat rate increases, sweat sodium concentration decreases [PMID
11171638],
77
plasma volume increases [PMID 9694425],
78
and during exercise in the heat there
is lowered heart rate and lowered rectal temperature [
PMID 9694427];
79
there is also a decrease
in perceived exertion as well as increased plasma volume [PMID 1763248].
80
Exertional heat
stress was found to cause decreased cognitive performance in soldiers, but not in soldiers who
had been heat-acclimated [PMID 17357764].
81
Mild exercise in severe heat conditions induces significant hyperkalemia. The level of
hyperkalemia is attenuated after acclimatization [
PMID 880177].
82
Men exercising in the heat
have an increased ability to conserve sodium after acclimatization [
PMID 880177].
83
Muscle
glycogenolysis is unaffected by acclimation during exercise in the heat [
PMID 8175568].
84
Likewise, the rate of gastric emptying does not appear to increase with heat acclimation [
PMID
2920721].
85
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
11
Acclimatization is accomplished by exposing individuals to heat stress over a period of
days or weeks. Exposure to heat for one hour or less, even with exercise, does not accomplish the
acclimatization possible with longer daily exposures [PMID 5853955].
86
Exposure to dry heat
increases sweat rate; exposure to humid heat stress results in a marked increase in sweat rate
[PMID 1763248].
87
Thus, acclimatization results in increased water requirements.
“TOUGHENING UP” PERSONNEL TO REQUIRE LESS WATER IN HEAT STRESS
CONDITIONS IS NOT POSSIBLE. Likewise, the idea that highly motivated individuals can
tolerate more heat stress exposure is also unjustified. In fact, they may push themselves to higher
activity levels while under heat strain, and thus HIGHLY MOTIVATED INDIVIDUALS MAY
BE MORE LIKELY TO INCUR SERIOUS HEAT INJURY [PMID 10063810].
88
Daily heat exposure is the most effective acclimation (i.e., laboratory chamber controlled
exposures to heat) strategy [PMID 11318020].
89
Intermittent heat exposure causes only minimal
heat adaptation [PMID 11318020].
90
Although 50% improvement in heat tolerance can be
derived from 8-11 weeks of training under temperate conditions (21° C), “intense training in a
cool environment cannot serve as a substitute for exercise in the heat if acclimation is desired
within a 2 week period” [PMID 481157].
91
Full acclimatization may take several weeks, but two
thirds or more of the adaptation is obtained within 5 days [PMID 9694427].
92
Optimal
acclimatization can be accomplished in 9 days [PMID 5853955],
93
although some changes
occurring during acclimatization (for example, plasma volume initial expands and then contracts)
continue for up to 3 weeks [PMID 1763248].
94
Even after 10 days of acclimatization, individuals
may have difficulty performing tasks requiring the acquisition of new behaviors [PMID
6626079].
95
Prolonging heat acclimatization from 6 to 12 days did not reduce the physiological
strain and limitation of heat-exercise tolerance imposed by wearing NBC protective clothing
[PMID 7588688].
96
However, when wearing normal combat clothing, acclimation responses
were greater after 12 than after 6 days of heat acclimation [PMID 7588688].
97
The psychological
strain from wearing protective clothing during vigorous exercise is not reduced by heat
acclimation or by endurance training because increased sweat accumulation adds to discomfort
[PMID 9520629],
98
[PMID 8039520].
99
Heat acclimatization occurs more rapidly in persons with greater cardiopulmonary fitness
[PMID 1763248].
100
Active women may acclimatize to heat at a faster rate or to a greater extent
than active men [
PMID 7085415].
101
Physical conditioning is also advantageous in the body’s response to dehydration, a heat
stress-related condition. In one study, physical conditioning was associated with enhanced work
performance during dehydration [PMID 11055570].
102
Inactivity results in decreased acclimatization after only a few days or weeks [PMID
1763248].
103
Exposing heat-acclimatized individuals regularly to cold temperatures (e.g., 4 hours
daily for 21 days) can cause a significant loss in heat acclimatization [
PMID 4004678].
104
A
single exercise and/or heat exposure per week was not different from complete cessation of
endurance exercise in the heat with regard to loss of acclimatization-related changes in plasma
volume [
PMID 3699011].
105
Acclimatization-related changes in sweat gland function may be
attenuated by increases in central dopaminergic activity [PMID 3397041].
106
Percent Achievement On Acclimatization
Physiologic Parameters
Day 1 Day 7 Day 14 Day 21
Rectal Temperature 6 38 72 100
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
12
Tympanic Membrane Temperature 6 37 71 100
Deep Esophageal Temperature 51 82 93 100
Mean Skin Temperature 80 93 98 100
Heart Rate 8 37 67 100
Systolic Blood Pressure 11 38 56 100
Diastolic Blood Pressure 7 36 70 100
Pulse Pressure 9 36 63 100
Mean Arterial Blood Pressure 4 35 79 100
Est. Total Vascular Resistance 8 37 70 100
Est. Cardiovascular Reserve 7 36 69 100
Sweat Rate 3 37 76 100
Urine Osmolality 3 39 82 98
Overall Percent Achievement
13 45 78 99.6
From U.S. Navy research in 1976, contained in previous edition of NAVMED P-5010. Manual of Naval
Preventive Medicine: Chapter 3: Ventilation and Thermal Stress Ashore and Afloat: Section III.
Physiological Principles 3-9. Effects of Heat.
Table 1 - Percent Optimum Heat Acclimatization
C2.3.13. Hydration Status
Water is essential to body cooling through the evaporation of sweat, as well as to routine
physiologic processes unrelated to heat stress.
C2.3.13.1. Eu-, Hypo-, De-, and Hyper-hydration
C2.3.13.1.1. Euhydration
Euhydration refers to a normal level of hydration (body water).
C2.3.13.1.2. Hypohydration
Hypohydration is having lower than normal body water (i.e., dehydration). It is
sometimes used to refer only to dehydration induced prior to exercise (by limiting fluid intake,
increasing urination, etc.). It is the result of inadequate fluid replacement.
Hypohydration increases heat storage by reducing sweating rate and skin blood flow
responses for a given core temperature [
PMID 11282312].
107
C2.3.13.1.3. Dehydration
Properly speaking, dehydration refers to the process (rather than the state) in which total
body water is decreased [USARIEM].
108
In common use, dehydration is used interchangeably
with hypohydration. The term is sometimes used to connote body water deficit caused by
exercise with inadequate water replacement. Dehydration increases body temperature (body
temperature increases approximately 0.18°F or 0.1°C for every percent of body weight
dehydration [
PMID 3569240]).
109
C2.3.13.1.4. Hyperhydration
Hyperhydration is increased total body water: consuming more water than is required by
the thirst mechanism (in the absence of increased sweating or other increased water loss).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
13
C2.3.13.2. Water Intoxication
Water intoxication refers to symptomatic hyperhydration. It may occur with moderately
increased fluid intake over the course of hours, or with greatly increased fluid intake (for
example, more than 5 liters/hour), with hyponatremia, pulmonary edema, and cerebral edema. It
has lead to death in military trainees [PMID 12053855]
110
[PMID 10091501].
111
This has led to a
maximum fluid intake recommendation of 1.5 liters/hour. Note: water loss of 2.5 liters/hour
during strenuous athletic competition has been documented. While replacement of such water
loss is essential, it should be done with caution and, preferably, with supervision.
C2.3.13.3. Hydration Status and Performance
Aerobic exercise tasks are likely to be adversely affected by heat stress and
hypohydration [
PMID 9694412].
112
Intermittent sprinting performance is poorer in a
hypohydrated compared with a euhydrated state [PMID10331887].
113
Even low levels of
dehydration (2% loss of body weight) impair cardiovascular and thermoregulatory response to
heat stress and reduce the capacity for exercise [PMID 9694419].
114
Rectal temperature rise was
found to be significantly greater and exercise tolerance time significantly decreased in
hypohydrated subjects exercising in the heat [PMID 9459534].
115
Esophageal temperatures
likewise rise more in hypohydrated subjects exercising in heat stress conditions [PMID
2361893].
116
Experiments have documented a lowering of cardiac stroke volume with
dehydration [PMID 10666060].
117
The rate of fluid loss may exceed the capacity of the gastrointestinal tract to assimilate
fluids [PMID 11547892].
118
Gastric emptying may be below the rate of fluid loss, and training to
drink during exercise has been recommended by at least one author as a way to enhance
tolerance of large amounts of oral rehydration liquids during exercise in heat stress conditions
[PMID 11547892].
119
Greater severity of heat strain is associated with lower rates of gastric
emptying [PMID 2920721].
120
Hyperhydration provides no advantages over euhydration regarding thermoregulation and
exercise performance in the heat [PMID 11282312].
121
Over-hydrating or meeting fluid needs
during very long-lasting exercise in the heat with low or negligible sodium intake can result in
reduced performance and, not infrequently, hyponatraemia [
PMID 11547892].
122
C2.3.14. Medications, Including Prescription and Non-Prescription Medications, Drugs
of Abuse, Folk Remedies, and Dietary Supplements
Dietary supplements are generally of no help or are detrimental to toleration of heat
stress, especially heat stress associated with exercise. Caffeine is not of ergogenic benefit in
endurance races during high heat stress [PMID 8781869].
123
Other stimulants, such as
pseudoephedrine, have had detrimental health effects when used in heat stress conditions
(including at least one case report of use associated with heat stroke [PMID 1943966])
124
and
should be avoided in such conditions [
PMID 10050577].
125
Ephedrine alkaloids (amphetamine-
like compounds derived from various species of herbs of the genus ephedra, also referred to as
Ma Huang, Ma-huang, or Ephedra equisetina) and creatine may contribute to subclinical
dehydration and heatstroke in selected individuals [PMID 12182766].
126
Cocaine can cause hyperthermia, largely through impaired heat dissipation. Even a small
dose of intranasal cocaine prior to heat stress impairs sweating and cutaneous vasodilation and
heat perception [PMID 12044126].
127
Cocaine has been associated with heat stroke in the U.S.
Navy.
128
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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Bromocriptine has been found to attenuate sweat gland function responses to
acclimatization [PMID 3397041].
129
Antihistamines and other anti-cholinergic drugs (including
atropine, found in the Mark I chemical warfare treatment injector, and scopolamine) may inhibit
sweating. Pyridostigmine (an anticholinesterase pre-treatment against nerve agents) may increase
rather than decrease sweating; however, the effect of pyridostigmine on heat stress tolerance is
unknown.
Antihypertensive medications may affect heat stress tolerance. Nonselective beta-
blockers may increase predisposition to exertional hyperthermia [PMID 1679517].
130
However,
one study demonstrated that although forearm blood flow was diminished by beta-blockers,
rectal temperature was not significantly increased, possibly due to increased sweating from beta-
blockade [PMID 2820920].
131
Diuretics may cause electrolyte (including sodium) loss. Diuretics
and laxatives can cause water loss, leading to dehydration.
Lithium may cause water loss (through diabetes insipidus) [PDR.net]
132
[PMID
11246113].
133
C2.3.15. Alcohol
(See the section on the effect of Alcoholic Beverages on heat stress response.)
C2.3.16. Activity, Rest, and Sleep
The heat generated by metabolism can be greatly affected by a person’s activity level, as
muscle contraction generates a large amount of heat (oxygen metabolism increases more than
20-fold [PMID 2583157]).
134
Unfortunately, activity level is not always totally voluntary (for
example, emergency maneuvers), and the body is not sufficiently sensitive to its need to decrease
activity-related heat production (the body is slow to recognize it needs to cool down). A person
may run in hot weather, for example, and by the time he or she feels “too hot,” he or she may
have already reached a point of needing complete rest to cool sufficiently or even may suffer
heat injury in spite of complete rest [Time].
135
Doing work in heat stress can cause core body temperature elevations. Intermittent rest
times with adequate replacement fluid availability usually can prevent temperatures from
becoming elevated. However, extremely high temperatures, heavy gear or clothing (such as
MOPP gear), or high work levels may require removal from heat stress (such as resting in an air
conditioned space and/or removal of MOPP gear) for adequate core body temperature control.
Rest cycles must be lengthened the higher the work levels and the higher the heat stress
conditions, even requiring resting more than 2 hours after only 15 minutes of work—or working
less than 15 minutes if shorter rest periods are anticipated [
PMID 10414066].
136
Work-rest cycle
times and fluid replacement requirement charts have been developed for work in heat stress in
humid and dry climates. The following is adapted from work done on laboratory acclimated
subjects [PMID 10414066].
137
Easy Work (250 W) Moderate Work (425 W) Hard Work (600 W)
WBGT
Index
(°F)
Work-Rest
(minutes)
Water Intake
(quarts/hour)
Work-Rest
(minutes)
Water Intake
(quarts/hour)
Work-Rest
(minutes)
Water Intake
(quarts/hour)
78-81.9 Unlimited 0.5 Unlimited 0.75 40/20 0.75
82-84.9 Unlimited 0.5 50/10 0.75 30/30 1.0
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
15
85-87.9 Unlimited 0.75 40/20 0.75 30/30 1.0
88-89.9 Unlimited 0.75 30/30 0.75 20/40 1.0
90+ 50/10 1.0 20/40 1.0 10/50 1.0
Table 2 - Work-Rest Cycles and Fluid Replacement for 4 Hour Periods
MOPP gear adds 10° F to the WBGT Index for Easy Work and adds 20° F to the WBGT Index for Moderate and
Hard Work; body armor adds 5° F to the WBGT Index
Rest = sitting or standing, in shade if possible.
Individual water needs vary by 0.25 quarts/hour.
Fluid intake should not exceed 1.5 quarts per hour; daily fluid intake generally should not exceed 12 quarts (note:
this is not to suggest limiting fluid intake by highly conditioned persons, who may require greater than 12 quarts
daily).
C2.3.16.1. PHEL Curves
Physiological Heat Exposure Limits (PHEL curves) identify the maximal allowable
exposure time or “stay time” for all U.S. Navy shipboard personnel when working in the heat
(OPNAVINST 5100.19 series Appendix B2-A).
138
Six categories of heat stress (PHEL curves I-
VI, shown in Figure 2) with different exposure times are used to protect against heat stress
injuries. The correct PHEL curve is determined by considering the WBGT index (rounded up to
a whole number) and the work entailed by a particular job, ranging from light work (PHEL
Curve I) to heavy work (PHEL Curve VI). The PHEL curves were developed and are accurate
for normal, healthy personnel who have had adequate rest (6 hours continuous sleep in the last
24 hours), adequate water intake, adequate recovery time from previous heat-stress exposure (2
hours recovery for every 1 hour exposure or 4 hours maximum), and full acclimatization to the
present heat stress environment. Personnel are assumed to be wearing clothing consisting of at
least 35 percent cotton fiber, not containing starch, and readily permeable to water transfer. The
limits presume that no prior heat injury or predisposing condition is present and that no
cumulative heat fatigue exists prior to re-exposure. PHELs are maximum allowable standards
and should be applied only in cases of short-term work exposures of up to 8 hours duration.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
16
Figure 2 - PHEL Curves
Exposure Time (Hrs)
125
120
115
110
105
100
95
90
85
80
012345678
I
II
III
IV
V
VI
WBGT Index (F)
PHEL CHART
(Curves I - VI)
Non-routine operations, such as performing operations in out-of-normal plant
configurations, increases in normal watchstander work rate, and minor equipment casualties
require the use of the next higher number curve. The presence of fuel vapors or combustion
gases greatly reduces the safe exposure times (to approximately one-third). Stay times based on
PHEL curve and work effort are shown in Table 3.
PHEL Curves
Total Exposure Time in Hours:Minutes
Without the presence of fuel vapors or
combustion gases
With the presence of fuel vapors or
combustion gases
WBGT
Index
(F)
I II III IV V VI I II III IV V VI
80.0
81.0
82.0
83.0
84.0
85.0
86.0
87.0
88.0
89.0
90.0
91.0
92.0
93.0
94.0
>8:00
>8:00
>8:00
>8:00
>8:00
8:00
8:00
7:25
6:45
6:10
5:40
5:15
4:50
4:25
4:05
>8:00
>8:00
>8:00
8:00
8:00
7:45
7:05
6:30
5:55
5:25
5:00
4:35
4:10
3:50
3:35
>8:00
>8:00
8:00
7:45
7:05
6:30
5:55
5:25
4:55
4:30
4:10
3:50
3:30
3:15
3:00
8:00
7:45
7:05
6:25
5:55
5:20
4:55
4:30
4:05
3:45
3:25
3:10
2:55
2:40
2:25
6:35
6:00
5:25
4:55
4:30
4:05
3:45
3:25
3:10
2:50
2:40
2:25
2:15
2:00
1:50
4:30
4:05
3:40
3:20
3:05
2:50
2:35
2:20
2:10
2:00
1:50
1:40
1:30
1:25
1:15
4:50
4:25
4:00
3:40
3:20
3:00
2:45
2:30
2:20
2:05
1:55
1:45
1:35
1:30
1:20
4:15
3:50
3:30
3:10
2:55
2:40
2:25
2:10
2:00
1:50
1:40
1:30
1:25
1:20
1:10
3:30
3:10
2:55
2:40
2:25
2:10
2:00
1:50
1:40
1:30
1:25
1:15
1:10
1:05
1:00
2:55
2:40
2:25
2:10
2:00
1:50
1:40
1:30
1:25
1:15
1:10
1:05
1:00
0:55
0:50
2:15
2:00
1:50
1:40
1:30
1:25
1:15
1:10
1:05
1:00
0:55
0:50
0:45
0:40
0:35
1:30
1:20
1:15
1:10
1:00
0:55
0:50
0:45
0:40
0:40
0:35
0:30
0:30
0:25
0:25
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
17
PHEL Curves
Total Exposure Time in Hours:Minutes
Without the presence of fuel vapors or
combustion gases
With the presence of fuel vapors or
combustion gases
WBGT
Index
(F)
I II III IV V VI I II III IV V VI
95.0
96.0
97.0
98.0
99.0
100.0
101.0
102.0
103.0
104.0
105.0
106.0
107.0
108.0
109.0
110.0
111.0
112.0
113.0
114.0
115.0
116.0
117.0
118.0
119.0
120.0
121.0
122.0
123.0
124.0
125.0
3:45
3:25
3:10
2:55
2:40
2:30
2:20
2:10
2:00
1:50
1:40
1:35
1:30
1:20
1:15
1:10
1:05
1:00
0:55
0:55
0:50
0:45
0:45
0:40
0:35
0:35
0:35
0:30
0:30
0:25
0.25
3:15
3:00
2:45
2:35
2:20
2:10
2:00
1:50
1:45
1:35
1:30
1:25
1:15
1:10
1:05
1:00
1:00
0:55
0:50
0:45
0:45
0:40
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0.20
2:45
2:30
2:20
2:10
2:00
1:50
1:40
1:35
1:25
1:20
1:15
1:10
1:05
1:00
0:55
0:50
0:50
0:45
0:40
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0.20
2:15
2:05
1:55
1:45
1:40
1:30
1:25
1:15
1:10
1:05
1:00
0:55
0:50
0:50
0:45
0:40
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0.15
1:45
1:35
1:25
1:20
1:15
1:10
1:05
1:00
0:55
0:50
0:45
0:45
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:15
0:10
0:10
0.10
1:10
1:05
1:00
0:55
0:50
0:45
0:45
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:10
0:10
0:10
0:10
0:10
0:10
0:10
0:05
0.05
1:15
1:10
1:10
1:05
0:55
0:50
0:45
0:40
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
1:05
1:00
0:55
0:50
0:45
0:45
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:10
0:10
0:55
0:50
0:45
0:40
0:40
0:35
0:35
0:30
0:30
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:15
0:10
0:10
0:10
0:10
0:45
0:40
0:40
0:35
0:30
0:30
0:25
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:10
0:10
0:10
0:10
0:10
0:10
0:05
0:35
0:30
0:30
0:25
0:25
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:10
0:10
0:10
0:10
0:10
0:10
0:05
0:05
0:05
0:05
0:05
0:20
0:20
0:20
0:15
0:15
0:15
0:15
0:10
0:10
0:10
0:10
0:10
0:10
0:05
0:05
0:05
0:05
0:05
0:05
0:05
0:05
0:05
0:05
Table 3 - Safe Exposure Times Aboard Ship
Changes in WBGT, work level or recovery time require re-calculating the remaining safe
stay time. The following equation may be used:
RSST = [(1 -(Et -R/2) / Atl)] x At2
Where:
RSST = remaining safe stay time (in minutes)
Et = elapsed time on station (in minutes)
R = recovery time in a cool environment (in minutes)
Atl = allowed PHEL time in first environment (in minutes)
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
18
At2 = allowed PHEL time in second environment (in minutes)
Adding intermittent rest times may extend the amount of time personnel can stay “on the
job.” However, exercise-rest cycles do not alter physiologic tolerance to uncompensable heat
stress [PMID 11252069].
139
It is to be noted that PHEL curves apply only to shipboard use (see
OPNAVINST 5100.19 series).
C2.3.16.2. Flag Conditions and Activity Limitations
The Navy uses a set of flags to indicate when certain heat stress hazards exist (Table 4).
These are based on the Marine “Heat Condition Flag Warning System” (Enclosure 4 of Marine
Corps Order 6200.1E).
140
WBGT Index Activity Level Hazards and Limitations Flag
Less than 80
Extremely intense physical exertion may precipitate heat exhaustion
or heat stroke.
White
80 - 84.9
Discretion is required in planning heavy exercise for unacclimatized
personnel.
Green
85 - 87.9
Curtail strenuous exercise and activity for unacclimatized personnel
during the first 3 weeks of heat exposure. Avoid classes in the
sun.
Yellow
(Amber)
88 - 89.9
Strenuous exercise must be curtailed for all personnel with less than
12 weeks training in hot weather.
Red
90 or above
Physical training and strenuous exercise must be suspended for all
personnel (excludes operational commitment not for training
purposes).
Black
Table 4 - Flag Conditions and WBGT
C2.3.16.3. Screening criteria for Heat Stress Exposure Ashore
While the flag system communicates heat stress conditions in a local geographic area, it
does not identify job-specific or work area-specific heat stress conditions. For example, WBGT
may be 75° F (23.9° C) outdoors at a Navy installation (white flag conditions), but the laundry
workers could be working indoors with a WBGT of 88° F (31.1° C). The following table is
adapted from the ACGIH 2005 TLVs and BEIs [ACGIH].
141
Acclimatized Unacclimatized
Work
Demands
Light Moderate Heavy Very
Heavy
Light Moderate Heavy Very
Heavy
100% Work 85.1 81.5 78.8 81.5 77 72.5
75% Work
25% Rest
86.9 83.3 81.5 84.2 79.7 76.1
50% Work 88.7 85.1 83.3 81.5 86 82.4 79.7 77
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
19
50% Rest
25% Work
75% Rest
90.5 87.8 86 85.1 87.8 84.2 82.4 79.7
Table 5 - Screening Criteria for Heat Stress Exposure (ACGIH) based on WBGT
For woven cloth overalls add 6.3° F (3.5° C) to the WBGT. For double-cloth overalls add 9° F (5° C) to the WBGT.
C2.3.16.4. Muscle Performance in Heat Stress conditions
Intermittent supramaximal running performance in the heat is reduced, which is not
caused by greater muscle glycogenolysis or lactate accumulation [PMID10331887].
142
Heat
stress reduces maximum metabolic rate (VO
2
max) [PMID 4039255],
143
[PMID 8175568].
144
Acclimatization and aerobic fitness increase VO
2
max, but a reduction in VO
2
max is still caused
by heat stress [PMID 4039255].
145
C2.3.16.5. Sleep Deprivation and Heat Tolerance
Sleep loss reduces heat tolerance [PMID 1763248].
146
C2.3.17. Mean Metabolic Rate
The mean metabolic rate is a value referred to in some scientific reports related to heat
stress. It is generally restricted to use in research.
C2.3.18. Attributes of Surrounding Materials
In one study, skin temperature and moisture were affected by the material or construction
of furniture coverings, although test subjects attributed personal thermal comfort more to room
climate than to material properties of furniture coverings [PMID 7148203].
147
Cotton continues
to be the preferred clothing material during hot weather. Special evaporative polyester fabric
clothing compared to cotton clothing does not alter physiological, thermoregulatory, or comfort
sensation responses during exercise in a moderately warm environmental condition [PMID
11740309].
148
C2.3.19. Motor Vehicles
On days when temperatures exceed 86° F (30° C), the temperature inside vehicles can
quickly reach 134° F to 154° F (56.7° C to 67.8° C). On clear sunny days, even with lower
temperatures (72° F, or 22.2° C), temperatures inside vehicles can reach 117° F (47.2° C).
Temperatures increase approximately 40° F (22.2° C), at an average rate of 3.2° F (1.8° C) per 5
minutes; 80% of the temperature rise occurs during the first 30 minutes. Opening (“cracking”)
windows 1.5 inches does not significantly decrease the rate of temperature rise in vehicles or the
final maximum internal temperature [
PMID 15995010].
149
C2.3.20. Electric Blankets
Cases of heat stroke (including two fatal cases) in users of electric blankets have been
reported; first and second degree burns were noted in the victims [
PMID 17133030].
150
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
20
C2.4. Heat Stress Vs. Heat Strain
C2.4.1. Heat Stress
Heat stress refers to the combination of all of those factors which result in heat gain (or
loss) to the body. Heat stress is the force or load acting upon the body. At a cellular level, cells
produce heat-shock (stress) proteins, increased levels of which induce transient tolerance to a
second heat stress [PMID 12075060].
151
Heat-shock protein production may play a role in
acclimatization [PMID 9375300].
152
At the tissue level, there is an acute-phase response to heat
stress that protects against tissue injury and promotes repair [PMID 12075060].
153
The oxidation
rate of ingested carbohydrates is reduced and muscle glycogen utilization is increased during
exercise in the heat compared with a cool environment [PMID 11896023]
154
[PMID
11219501].
155
C2.4.2. Heat Strain
Heat strain is the resulting abnormality or “distortion” of the body’s physiology when
exposed to more heat stress than the body is prepared to compensate for at that time. The
extreme result is the failure of the body to cool itself (thermoregulation failure), and core
temperature rises (often precipitously).
Heat increases myocardial oxygen demand. Electrocardiogram (EKG) changes may
include increased J-point displacement (J wave, also seen in hypothermia [Wagner]),
156
S-T
segment flattening (0.08 s), and prolongation of the Q-T interval with reduction in T-wave
amplitude [PMID 7362568].
157
Figure 3 - J Wave Appearance on Electrocardiogram
Mental performance is also affected by the heat. The following graph illustrates the
impact on mental performance of heat stress exposure. [HEW].
158
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
21
Figure 4- Upper Limits of Exposure for Unimpaired Mental Performance
Heat stress decreases cerebral blood velocity and increases cerebral vascular resistance,
and physiologic responses to orthostatic challenges (e.g., increasing heart rate and blood pressure
on standing up) are blunted under heat heat stress [PMID 16763078],
159
[PMID 16916922].
160
Severe heat stress has been noted to cause an imbalance of oxidant production and
antioxidant defense (what has been called “oxidant stress”), which may lead to oxidant-mediated
injury to muscle cells [PMID 10601884].
161
The recommended threshold WBGT Index value for instituting hot weather practices is
75° F or 23° C [CHPPM].
162
C2.5. Prevention Of Heat Stress Injuries
Heat stress injuries and illnesses are preventable threats to health. In the United States,
annual heat-related deaths between 1979 and 1996 ranged from 148 to 1,700 [MMWR].
163
The
U.S. Army had 196 hospitalizations due to heat illness or injury (“excessive heat”) in 1994, with
a rate of 0.36 per thousand per year, while the U.S. Air Force had 19 such hospitalizations
[
AMSUS].
164
From 1981 to 1991, an average of 135 British servicemen and women were
hospitalized yearly for heat-related conditions [PMID 8904496].
165
C2.5.1. Primary Prevention
Primary prevention of heat stress injuries (i.e., preventing them from occurring) is
accomplished by recognizing and mitigating significant heat stress conditions and by identifying
and taking steps to compensate for risk factors of heat stress injury. The main elements of
primary prevention consist of adequate hydration (see
Drinks, above), light clothing, and
appropriate exercise or work limitations for the level of heat stress and PPE used (see PHEL
Curves
, above).
C2.5.2. Secondary Prevention
Secondary prevention of heat stress injuries (i.e., treating them as early as possible)
includes prompt recognition and treatment, with appropriately aggressive cooling as necessary.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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C2.5.3. Tertiary Prevention
Tertiary prevention of heat stress injuries (limiting disability) consists of avoiding re-
exposure to heat stress conditions after heat stress over-exposure has occurred. Medical
clearance should be required before heat stress re-exposure if there has been a previous history of
heat stress injury. After recovery, a customized gradual acclimatization process to redevelop heat
tolerance may be successful. Such a process may take up to a year, and in some cases may not be
possible [PMID 2406545].
166
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INDIVIDUAL FACTORS ENVIRONMENTAL FACTORS
Advanced age
Alcohol use
Antihistamine use
Bromocriptine use
Cocaine use
Heavy clothing, including MOPP gear
High body mass index
Insufficient sodium (salt) intake
Insufficient water replacement
Lack of acclimatization
Lack of sufficient available water
Lack of sufficient rest
Poor physical conditioning (“out of shape”)
Prior heat stress injury
Respirator use
Sleep loss
Stimulants
Strenuous activity (exercise or labor)
Sunburn
Underlying illness (including infections,
such as gastroenteritis, and chronic
diseases, such as diabetes mellitus,
cardiovascular disease, and congestive
heart failure)
Use of supplements/boosters such as
Ephedra, Ephedrine, Ma Huang, and
Guarana
Young age (<5 years [PMID 2371104])
167
High temperature (>85° F)
High humidity
Midday
Hot large objects nearby (close enough to
provide significant radiant heat)
No air movement (wind speed = 0)
Deep mines
Table 6 - Heat Stress Injuries—Risk Factors and Predisposing Conditions
C2.6. Temperature Measurement And Thermometers
C2.6.1. Skin Temperature
Skin temperature is affected by dermal blood flow and environmental conditions, and is a
poor indicator of body core temperature. Skin temperature is unreliable in the diagnosis of heat
stress injury severity [
PMID 2805574].
168
C2.6.2. Expired Breath
Expired breath temperature does not correlate with body core temperature, even after
holding a breath for 30 seconds [
PMID 11007321].
169
C2.6.3. Oral Thermometers
Oral thermometers are popular and give a reasonable approximation of body temperature
(usually reading lower than core temperature) in many circumstances. Recent drinking of hot
(within 5 minutes [PMID 11606822])
170
or cool (within 30 minutes [PMID 11606822],
171
[PMID
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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3722670])
172
food or liquids, mouth breathing, improper technique, shock, and heat injury may
affect either oral temperature readings or the amount they reflect true core body temperature.
Oral thermometers should not be depended upon to diagnose heat stress injuries or to guide
therapy of heat stress injuries.
C2.6.4. Tympanic (Ear) Electronic Thermometers
Tympanic (ear) electronic thermometers can significantly underestimate core
temperatures. Readings may be affected by external conditions (such as facial fanning [PMID
9116786]),
173
liquids in the ear canal (e.g., cold water used in cooling), and improper technique.
Thus, tympanic thermometers do not reliably measure core body temperature and their use for
this purpose is not recommended. The use of fiber optic devices may overcome the affect of
some of those factors [PMID 9729565].
174
C2.6.5. Rectal Temperature
Rectal temperatures generally are a good reflection of core body temperature. However,
with aggressive cooling techniques, readings may lag behind actual core body temperature
[PMID 1608386].
175
Thus, if used during aggressive treatment of heat injuries, caution must be
exercised not to over-treat (over-cool).
C2.6.6. Esophageal Thermometers
Esophageal thermometers give accurate core body temperature measurements. They are
more difficult to use than oral, rectal, or ear thermometers, and may not be readily available.
Readings in patients with tracheal intubation may be affected by placement of the thermometer
and temperature of inspired air, especially in children [PMID 8478651]
176
Esophageal
temperatures may fluctuate rapidly as a result of subjects swallowing liquids or saliva [PMID
6853278],
177
[PMID 5060664].
178
C2.6.7. Bladder Temperature
Bladder temperatures can accurately indicate core body temperature during anesthesia
without the lag during rewarming noted with rectal temperatures [PMID 9382206].
179
The use of
bladder temperatures may be restricted to advanced hospital settings under limited conditions.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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Chapter 3:
C3. Diagnosis of Heat Stress Injuries
All heat stress injuries are best recognized by having a high index of suspicion in
appropriate settings. Hot climates and high humidity conditions are obviously high-risk settings.
However, hot workspaces, inadequate fluid replacement, or the impact of protective equipment
may be less obvious to health care workers. Military cases of heat stroke, although more
common in summer, have occurred in the coldest part of the year [PMID 8904496].
180
The
possibility of a heat stress injury should be considered in any person with an elevated
temperature not due to another cause, or that has been in a heat stress situation. Specific
symptoms, signs, and findings noted below will give further guidance in the recognition of heat
injuries and illnesses. An algorithm (Figure 5) is available to assist in the diagnosis of heat stress
injury.
It is to be noted that heat stress injuries represent a continuum rather than discreet injury
categories. Also, not all signs and symptoms are always present for each heat stress injury.
Distinguishing the mildest from the most severe injuries is easy. However, heat stress injuries
may include signs and symptoms of more than one injury category. For example, a case of heat
exhaustion with confusion may be difficult to differentiate from heat stroke, and with inadequate
treatment may in fact become a case of heat stroke.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
26
Figure 5 - Acute Heat Exposed Patient Diagnostic Flow Chart
Four major types heat stress injuries are commonly recognized: heat rash, heat cramps,
heat exhaustion, and heat stroke. Some authors elaborate and include more heat exposure-related
conditions. An attempt is made here to include most such conditions.
Certain underlying conditions have specific symptoms that may be precipitated by
exposure to heat stress. Migraine headaches may be precipitated by heat (or cold) stress exposure
[PMID 6935858].
181
Intermittent hyperthyreosis is a condition in which hyperthyroid patients
during heat stress exposure experience various symptoms (insomnia, irritability, headache,
tension, tachycardia, palpitations, precordial pain, dyspnea, flushes with sweating or chills,
tremor, abdominal pain or diarrhea, polyuria, weight loss in spite of ravenous appetite, fatigue,
exhaustion, depression, weakness, lack of concentration and confusion) [PMID 52584]
182
[PMID
6935858].
183
Therapy is medical and related to treating the thyroid condition rather than oriented
at heat stress exposure control. Although migraines and intermittent hyperthyreosis may be
precipitated by heat stress exposure, they are not considered true “heat illnesses,” as they are
primarily unrelated (to heat) underlying conditions.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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C3.1.1. Heat Rash (Miliaria Rubra)
Heat rash has a number of other names, including prickly heat, sweat rash, lichen
infantum; lichen strophulosus; strophulus; summer rash; tropical lichen; lichen tropicus; wildfire
rash [Steadman’s].
184
It is a cutaneous reaction to heat stress exposure, with redness and
inflammatory skin reaction. It consists of papules and vesicles at sweat glands (
photo).
Symptoms include pruritus and a burning sensation, as well as heat intolerance [PMID
10994246].
185
Treatment is removal from heat stress exposure. Application of cool wet cloths may
alleviate symptoms. Cool starch baths, calamine lotion, corticosteroid lotion [Noojin],
186
sometimes with 0.25% menthol added [
Merck],
187
may also be tried if necessary. Oral
antihistamines to control itching have been suggested [Noojin],
188
but this should be limited to
use for severe itching in air conditioning, as caution must be used in hot environments as
antihistamines may inhibit sweating.
Miliaria can impair sweating and reduce heat tolerance. One study found that heat
intolerance due to heat rash was not resolved until after 21 days [PMID 7435594].
189
If miliaria
covers more than 8% of the body surface (e.g., one upper extremity, or half of a lower extremity,
or one quarter of the torso, or one half of the head and neck, etc.), re-exposure to heat stress
should be deferred until miliaria fully resolves.
C3.1.2. Erythema Ab Igne (Erythema Caloricum)
Erythema ab igne (erythema caloricum) is a reticulated erythematous hyperpigmented
eruption that occurs after localized chronic exposure to heat [PMID 9040977],
190
including
chronic exposure to heat from fires, chairs with built-in heaters, car heaters [PMID 9040977],
191
hot water bottles, infrared lamps, and heating pads [PMID 7845500].
192
Central heating and not
using open fires has largely reduced the incidence of erythema ab igne [PMID 7999279],
193
[PMID 7845500].
194
Occupational exposures causing this condition have included cooking
[PMID 1828060]
195
and baking [PMID 8772030].
196
While it has been noted to be a marker for
underlying disease, including cancer [PMID 4067962],
197
some authors have proposed a
pathogenic role for erythema ab igne [PMID 2685415]
198
(photo). Treatment is removal from the
heat source.
C3.1.3. Exertional Hyperthermia
Exertional hyperthermia refers to a significant (for example, greater than 0.9° F or 0.5° C) rise in
body temperature that occurs with exercise. It is not a diagnosis, but rather is used (usually by
researchers) to describe a physiologic response to exercise in heat stress conditions [PMID
10484593].
199
C3.1.4. Heat Syncope
Heat syncope (fainting) generally occurs when individuals that are not acclimatized are
exposed to heat stress, most often during the first 5 days of heat exposure [
PMID 1763248].
200
A
common scenario is when personnel are required to stand at attention or in formation in the heat.
It is syncope from vascular insufficiency (hypotension). Hypovolemia (due to diuretics or
medications decreasing vascular tone) increases risk of heat syncope [Nadel].
201
Symptoms are syncope and postural lightheadedness. Victims are tachycardic (in contrast
to the bradycardia expected in vaso-vagal syncope), have normal temperatures, are sweating, and
have postural hypotension.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
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Treatment is as for fainting: supine position, elevation of the feet, and oral fluids (those
containing sodium may be preferable). Recovery is expected to be prompt and complete.
C3.1.5. Heat Edema
Heat edema is dependent (lower extremity) edema that develops or worsens soon after
heat stress exposure (usually within 48 hours). It is probably hormonally mediated [Nadel].
202
Victims have swelling or increased pre-existent edema of the lower extremities. No specific
treatment is required, as the condition is expected to resolve as the acclimatization process
continues. In cases of excessive edema due to underlying disease, some authors recommend
removing the victim from further heat stress exposure, rather than giving diuretics to enable them
to complete heat acclimatization [Nadel].
203
C3.1.6. Heat Tetany
Heat tetany is the result of hyperventilation by an individual after being exposed to heat
stress. Respiratory alkalosis, resulting in decreased ionized serum calcium, may be the
underlying mechanism [Schmidt]
204
[PMID 2178579].
205
It generally occurs prior to
acclimatization. Symptoms include muscle spasm (local or generalized) and perioral numbness
and tingling. Victims are alkalotic, and blood work may show hypocarbia and high partial
pressure of oxygen (pO
2
). Treatment is temporary removal from heat stress. Some authors
recommend that workload be decreased before resuming acclimatization [Nadel].
206
C3.1.7. Heat Cramps
Heat cramps occur in heat-acclimatized individuals performing vigorous physical
exercise in heat stress conditions. Heat cramps in such a setting are thought to be due to
hyponatremia [PMID 8653105].
207
Continuous strenuous exercise in the heat, such as a several-
day sports tournament or building project, may eventually lead to decreased sodium and favor
development of heat cramps. Symptoms are cramps in the affected muscles (generally those
muscles that have been exercised), and other than the fatigue associated with the exercise, are not
accompanied by constitutional complaints. Treatment for heat cramps is increased sodium
intake, which has eliminated heat cramps even in highly competitive sport competition [PMID
8653105].
208
C3.1.8. Heat Exhaustion
Heat exhaustion has been defined both as simply “the inability to continue exercise in the
heat” [PMID 1763248]
209
(which could be taken to imply no distinct medical illness) and “a
form of reaction to heat, marked by prostration, weakness, and collapse, resulting from severe
dehydration” [Stedman’s]
210
(implying a distinct medical illness or injury). It is treated here as a
distinct medical illness or injury.
C3.1.8.1. Symptoms of Heat Exhaustion
Heat exhaustion is characterized by dizziness, weakness, or fatigue often following
several days of sustained exposure to hot temperatures, and results from dehydration or
electrolyte imbalance [
MMWR].
211
Heat exhaustion is a serious heat injury, and may be
classified according to the underlying physiologic mechanism as sodium depletion (ICD-9-CM
code 992.4, “heat exhaustion due to salt depletion”) or water deficient (ICD-9-CM code 992.3,
“heat exhaustion, anhydrotic”) [
WHO].
212
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29
C3.1.8.2. Sodium-depletion Heat Exhaustion
Sodium-depletion heat exhaustion occurs when individuals exposed to excessive heat
stress consume sufficient water but insufficient salt. Hyponatremia (low sodium levels, serum
sodium less than 130 mEq/L [
PMID 10530529])
213
may result from inadequate sodium in the
diet (a rare occurrence in American diets), excessive sodium loss in sweat (more likely to occur
prior to heat acclimatization), or water intoxication. Symptoms include nausea, vomiting,
diarrhea, headache, dizziness, weakness, alterations of mental status, and minimal or no thirst.
Seizures were noted in 31% of victims in a study involving Army trainees [
PMID 11370203].
214
The victim usually has cool, moist skin that may be sticky and pale, and often is hypotensive and
tachycardic with normal (or even low) body temperature and normal urine volume.
Hyponatremia always is present. The existence of hyponatremia is suggested by altered mental
status or by seizures without hyperpyrexia or hypoglycemia during prolonged exercise in the
heat [PMID 10530529].
215
Treatment of sodium-depletion heat exhaustion is removal of the victim to a cool place
and administration of sodium replacement (oral or IV fluids of normal or high tonicity, such as
NS or hypertonic saline) until symptoms clear and pulse and urine findings normalize (including
urine sodium content of at least 10 mEq/L). Although 1 to 2 liters of saline solution is usually
sufficient, up to 4 liters of IV fluids may be required [Schmidt].
216
Unless more fluid is needed to
maintain blood pressure, current clinical recommendation is to limit IV saline administered in the
field (i.e., pre-hospital) to 2 liters to avoid pulmonary edema [Noltkamper].
217
Heavy clothing
should be removed from patients and they should be allowed to rest in a shaded and ventilated
space, while active cooling is initiated (see Cooling, below). Heat exhaustion victims should
improve rapidly with shaded rest, cooling, and replacement of sodium. If sodium has been very
low (less than 120 mEq/L) for more than 48 hours, sodium replacement may lead to cerebral
edema if done too rapidly. In such cases, sodium replacement should be monitored [PMID
12074531]
218
or paced [Nadel].
219
In hyponatremia of shorter duration, sodium replacement can
be more rapid. Avoidance of aspirin and other non-steroidal anti-inflammatory agents has been
recommended to prevent possible paradoxical hyperthermia [Nadel].
220
C3.1.8.3. Water-deficient Heat Exhaustion
Water deficient heat exhaustion results from excessive heat stress with inadequate water
replenishment, usually due to unavailability of water. Heat exposure with increasing dehydration
progressively limits ability to tolerate heat, with virtually no ability to exercise in severe
dehydration (loss of body water of 7% of body weight) [
PMID 1763248].
221
Symptoms include
malaise, vomiting, confusion [PMID 12074531],
222
anxiety, weakness, agitation, and even
delirium [Nadel].
223
Victims are dehydrated, oliguric, hyperthermic (temperature of 100.4° F or
38° C or greater [PMID 8775579]),
224
and may exhibit hyperventilation and tetany.
Hypernatremia is characteristic. Heat stroke may be imminent with this heat stress injury.
Treatment is removal from heat (remove heavy clothing, move victim to a shaded,
ventilated area, begin active cooling, see Cooling, below) and emergent transport to a hospital
for water replacement. IV fluids should be used to replace volume (primarily) and lower serum
sodium (at 0.5 to 1 mEq/hour but no more than 10-15 mEq/24 hours, to avoid cerebral edema as
a result of decreasing sodium too rapidly). Initially, NS is appropriate until tissue perfusion is
restored, at which time 0.5NS or other hypotonic solution may be used. A target of 0.5 ml/kg
hourly urine output has been recommended [Londer].
225
Aggressive cooling should be instituted
if necessary to maintain core temperature less than 102° F (38.9° C).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
30
C3.1.9. Heat Stroke
Heat stroke is the most serious heat stress exposure-related illness (injury).
Unfortunately, early or impending heat stroke may go unrecognized [PMID 2910771].
226
It is
defined as a seriously elevated temperature (> 104° F or 40° C [
PMID 12075060])
227
that causes
CNS injury, caused by heat stress conditions beyond the compensatory (cooling) ability of the
body. It is a life-threatening emergent medical condition. Without prompt treatment, victims will
sustain permanent injury or death. Multiple organ dysfunction syndrome has been common in
some case series [
PMID 10229168].
228
C3.1.9.1. Classic Heat Stroke
Classic heat stroke is the most common type of heat stroke [
MMWR].
229
It generally
affects the elderly and those with underlying disease or other debilitating condition. It is most
common during summer months and tends to occur in outbreaks (e.g., associated with a “heat
wave”). Excessive heat, high humidity, decreased sweating, and dehydration are mechanisms
involved [Simon].
230
However, maximum daily temperature and humidity have not been found
to be good predictors of the number of heat stroke injuries [PMID 11235827].
231
• previous heatstroke
• age (the young and the elderly)
• social circumstances (e.g., living alone, the urban poor)
• medical history and chronic health conditions (e.g., cardiovascular disease,
respiratory diseases, schizophrenia with neuroleptic treatment [PMID 661049],
232
amyotrophic lateral sclerosis receiving nortriptiline, multiple sclerosis, attention
deficit disorder, cystic fibrosis [PMID 9167437],
233
hyperthyroidism [PMID
11510526])
234
• other conditions that might interfere with the ability to care for oneself
• alcohol consumption (which may cause dehydration)
• physical activity (e.g., exertion in exceptionally hot environments during work or
recreation—see Exertional Heat Stroke, below), specifically indoor activity with
malfunctioning air-conditioning [PMID 9167437]
235
• use of medications that interfere with the body's heat regulatory system, such as
neuroleptics (antipsychotics or major tranquilizers) and medications with
anticholinergic effects (e.g., tricyclic antidepressants, antihistamines, some
antiparkinsonian agents, and some over-the-counter sleeping pills) [
MMWR].
236
A
patient who developed hyperpyrexia and heat stroke after taking overdoses of a
monoamine oxidase inhibitor, benzodiazepines and a beta-adrenergic receptor
blocking agent has been described [
PMID 550464].
237
Heat stroke has also been
reported in a patient taking perphenazine and amitryptyline [
PMID 6842224]
238
Table 7 - Risk Factors for Classic Heat Stroke
C3.1.9.2. Exertional Heat Stroke
Exertional heat stroke is the type most likely to be encountered in active service
personnel. It tends to occur sporadically in young, active people. According to a recent article, it
is the third leading cause of death among American athletes [PMID 12172074].
239
Increased heat
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
31
production from exercising skeletal muscles is a major contributing mechanism [Simon].
240
Acute renal failure may occur in 25% of patients with exertional heat stroke [PMID 9351070].
241
While hot weather or surrounding conditions increase the heat stress on an individual, exertional
heat stroke has been documented in physically conditioned military personnel at ordinarily
comfortable temperatures, even below 75° F [PMID 2107465].
242
• sleep loss
• generalized fatigue [PMID 2406545]
243
• inappropriately heavy clothing
• exposure to direct sunlight
• dehydration
• lack of cardiovascular conditioning
• lack of acclimatization to heat [Simon]
244
• dehydration or lack of access to water
• underlying health problems (for example, sickle cell trait is associated with
exertional collapse and sudden death characterized by rhabdomyolysis, heat
stroke, and cardiac arrhythmia, and has a 40-fold increased risk of sudden death in
affected soldiers during military basic training [
PMID 8990839])
245
Table 8 - Predisposing Factors for Exertional Heat Stroke
Heat intolerance (inability to adapt to heat stress) occurs in a small percentage of prior
heatstroke patients, and may be transient or persistent [PMID 2406545].
246
Recovery from
exertional heatstroke is idiosyncratic and may require up to 1 year in severe cases [PMID
2406545].
247
In one study, no measured variable predicted recovery from exertional heatstroke,
or heat acclimation responses [PMID 2406545].
248
C3.1.9.3. Diagnosis of Heat Stroke
Symptoms and signs of heat stroke include feeling overheated, weakness, fatigue,
irritability, bizarre behavior, combativeness, hallucinations, loss of consciousness (often with
little or no prodrome), and coma. Victims occasionally have feelings of euphoria. Sweating may
or may not be present. Heat stroke victims frequently have diarrhea and vomiting. In exertional
heat stroke, metabolic acidosis is the predominant acid-base change, especially in victims
presenting with higher temperatures [PMID 2692177],
249
followed by respiratory alkalosis (a
study that may have included both exertional and classic forms of heat stroke found similar
results [PMID 11398693]).
250
In classic heat stroke, reports are inconsistent between metabolic
acidosis or respiratory
alkalosis as the predominant finding [PMID 2355761],
251
[PMID
12075060].
252
The hemodynamic changes in severe heat exposure reflect a hyperdynamic circulation
with tachycardia and high cardiac output [PMID 10517377].
253
In one study, relative
hypovolemia was more pronounced in patients with heatstroke compared to patients with heat
exhaustion; and. signs of peripheral vasoconstriction were more often present in patients with
heatstroke, while patients with heat exhaustion more often demonstrated peripheral
vasodilatation [
PMID 10517377].
254
Arrhythmias are common in heat stroke. One study of heat stroke patients found
prolonged Q-T interval (61 percent), sinus tachycardia (43 percent), diffuse nonspecific ST-T
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
32
changes (26 percent), conduction defect (22 percent), and ST-T changes consistent with
myocardial ischemia (21 percent) [PMID 8339628].
255
Pericardial effusion has been reported in
heat stroke [PMID 1452370],
256
[PMID 11496687].
257
When interpreting ST-T elevation in the
ECG of a heat stroke patient, caution should be used so as to not misdiagnose it as an acute
myocardial infarction [PMID 16043949].
258
Rhabdomyolysis is common in severe heat injury, with extremely high serum and urine
myoglobin and serum creatinine kinase concentrations (for example, 100 times normal levels).
(It is to be noted that exertion without heat stress injury may cause creatinine kinase levels of
nearly 5000 international units/liter [
PMID 9827835].)
259
Carboxyhemoglobin levels may be elevated in heat stroke, even without exposure to
carbon monoxide; elevated carboxyhemoglobin levels may be due to heat shock protein up-
regulation (specifically hemeoxygenase-1, classified as heat-shock protein 32) [
PMID
10088844].
260
Oxyhemoglobin is partially oxidized to met-hemoglobin in severe heat stress
conditions, but carboxyhemoglobin is resistant against heating [
PMID 11516900].
261
System Symptom, Sign, or Finding
CNS
• Delirium
• Coma
• Euphoria
• Hallucinations
• Rapid eye movement
• Tremors
• Tonic contractions
• Seizures
• Cerebellar dysfunction (dysarthria, ataxia, downbeat nystagmus [PMID
16311159])
262
• Hemiplegic episodes
• CNS hemorrhage
• Cerebrospinal fluid normal pressure, elevated protein levels to 150 mg/dl,
occasional pleocytosis
Liver
• Acute hepatic failure [
PMID 17226914]
263
• Serum transaminase elevation (100x normal not uncommon)
• Jaundice
• Hypoglycemia
Kidneys
• Acute renal failure
• Acute tubular necrosis (associated with rhabdomyolysis)
• Myoglobinuria
• Pyuria
• Proteinuria
• Microscopic hematuria
• Granular casts
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
33
System Symptom, Sign, or Finding
Muscles
• Cramps
• Rigidity
• Rhabdomyolysis
• Elevated serum myoglobin
• Hyperphosphatemia
• Hyperuricemia
• Elevated plasma creatinine kinase (CK)
Blood
• Coagulation abnormalities
• Altered clotting time and clot retraction
• Fibrinolysis
• Platelet count usually low
• Factors V and VIII usually low
• Purpura
• Conjunctival hemorrhages
• DIC
• White blood cell count may be 30,000 - 40,000/ul
Cardiovascular
• Sinus tachycardia (as high as 150 beats per minute)
• Widened pulse pressure
• Increased cardiac index or hypotension (late)
• Central venous pressure normal or elevated
• Moderate fluid requirement
• Right heart dilation
• Pericardial effusion
• EKG abnormalities (ST-segment depression, T-wave abnormalities, and
conduction disturbances)
GI
• Diarrhea
• Vomiting
• Mesenteric vascular constriction
• Local areas of mucosal ulcerations
• Hematemesis
• Melena
Pulmonary
• Hyperventilation
• Respiratory alkalosis
• Hemoptysis
• Pulmonary edema
Table 9 - Symptoms, Signs, and Findings in Heat Stroke
C3.1.9.4. Criteria for Making the Diagnosis of Heat Stroke
Heat stroke is diagnosed when there is severely elevated body temperature that causes
CNS injury. Clinically, it may be difficult to differentiate heat stroke from heat exhaustion with
impending heat stroke. Altered CNS function without injury may exist, and prior emergency
cooling may obscure an elevated temperature. The medical literature includes temperature
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
34
criteria for the diagnosis of heat stroke ranging from 103.1° F (39.5° C) [PMID 2406546]
264
to
105.8° F (41° C) [PMID 9694423].
265
HEAT STROKE SHOULD BE SUSPECTED IN ALL PATIENTS WITH ALTERED
MENTAL STATUS AND ELEVATED TEMPERATURE OR HIGH LEVELS OF EXERTION.
If other etiology is not apparent, it should be considered heat stroke until proven otherwise.
Rapid cooling should be instituted in such cases, while further studies (such as lumbar puncture,
etc.) are pursued.
The table in C6. Criteria for the Diagnosis of Heat Stroke may assist in the diagnosis of
heat stroke. (Note: criteria have been established for the diagnosis of heat stroke as a cause of
death [PMID 9095294].)
266
C3.1.10. Severe Exertional Heat Injury (“Exertional Heat Illness”)
Some severe cases of heat exhaustion have clinical and laboratory findings consistent
with heat stroke but without clear evidence of CNS injury. Cases of severe exertional heat illness
typically have rhabdomyolysis or other evidence of muscle, blood, kidney, liver, endocrine, or
blood injury. Confusion, often found in severe heat exhaustion as well as in heat stroke, is
generally transient, clearing readily and completely with treatment. The U.S. Army currently
uses the designation “exertional heat illness,” although the literature has used that term to include
all exertional heat stress illness. While such cases should be diagnosed as heat exhaustion,
treatment is similar to that for heat stroke. Again, heat injuries often show more of a continuum
of severity, rather than discreet diagnoses.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
35
Chapter 4:
C4. Treatment of heat stroke
C4.1. Treatment of Heat Stroke - General
Comprehensive emergency management of heat stroke is beyond the scope of this
manual. Specific critical issues are addressed here to give the health care provider a base of
understanding from which to make clinical decisions.
C4.1.1. Cooling
The goal in the treatment of heat stroke is rapid cooling to (theoretically) normal body
temperature. Clinically, to prevent over-cooling (reported to occur in 33% of heat stroke cases
[PMID 1608386]),
267
the target temperature of cooling is to 101° F (38.3° C) [Schmidt]
268
(literature reports range from 99.5° F [PMID 2692177]
269
to 102.2° F [PMID 10959266]).
270
Rapid cooling to less than 102° F (38.9° C) is associated with a significantly reduced mortality
rate [PMID 3741557].
271
To avoid “overshoot” (over-cooling), some clinicians clinical use a
target temperature of 102° F (38.9° C) when using aggressive cooling (e.g., iced water
immersion) and a rectal thermometer to monitor body core temperature; when the target
temperature is reached, a fan with cool misted water or a lukewarm shower may be used
[Noltkamper].
272
Cooling should be started immediately on diagnosing heat stroke or serious heat
exhaustion, preferably while the victim is being transported to the hospital. With the notation that
overcooling should be avoided, the more rapid the cooling, the lower the mortality [PMID
11510526]).
273
However, although important in determining prognosis, early treatment may not
prevent severe complications [PMID 10959266].
274
Cooling may be done through three mechanisms: cooling the skin while maintaining
cutaneous blood flow, cooling internal organs directly, and cooling blood directly by removal,
cooling, and re-introduction of blood.
1) Cooling the skin while maintaining cutaneous blood flow
C4.1.1.1.1. Clothing Removal
Unless prohibited by operational personal protection requirements (e.g., battle, chemical
or biological or radiological threat), the victim’s clothing should be removed immediately.
C4.1.1.1.2. Fanning
Cooling with large amounts of airflow is often the only effective cooling method
immediately available. Helicopter downdraft cooling has been used successfully on heatstroke
victims [
PMID 3579826].
275
C4.1.1.1.3. Cold or Ice Water Immersion
IMMERSION OF THE VICTIM IN COLD OR ICE WATER IS THE MOST
EFFECTIVE TREATMENT TO RAPIDLY DECREASE CORE TEMPERATURE, AND
SHOULD BE PERFORMED IMMEDIATELY [PMID 9366461,
276
PMID 15248787].
277
As
heat stroke victims may be shunting blood from the skin, and as cooling causes cutaneous
vasoconstriction, effort may be necessary to restore or increase cutaneous blood flow. Cold or ice
water immersion techniques are labor-intensive. Vigorous rubbing of the skin, or intermittent
warm air or warm water exposure is done to maintain cutaneous blood flow.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
36
As reflex hyperemia is a transient early reaction to ice water immersion, a protocol of
intermittent immersion (e.g., suspending the patient over ice water and repeatedly immersing or
soaking them)
278
may be effective at cooling the victim while avoiding the need for rubbing the
skin. Immersion times can be adjusted for the victim, but example initial times may be 2 minutes
in, 1 minute out.
Care must be exercised to avoid water inhalation by the patient. Vomitus, urine, blood,
and fecal material may soil the water, requiring universal (isolation) precautions and making IV
access and site care more difficult. Also, immersion baths must be disinfected between patients,
and water in the ear canals may cause inaccurate tympanic thermometer readings.
C4.1.1.1.4. Cold Packs, Cooling Blankets, Fanning, Mists, Cooling Units
One alternative to cold or ice water immersion is the application of cold packs or ice
packs or ice water slush to part of the body. Another alternative is the use of cooling blankets
(blankets with tubing containing a circulating coolant), which cool the patient without wetting.
However, contact area with the body is less than can be achieved with immersion. They are
unlikely to be available in a field situation. Evaporative cooling techniques may also be used,
including fanning the patient with or without water or mist, and using a “body cooling unit” (a
special bed spraying water at 59° F or 15° C and blowing air at 113° F or 45° C) [PMID
12075060].
279
2) Cooling internal organs directly
Ice water NG lavage and/or ice water enemas may be used to rapidly cool the body. Iced
peritoneal lavage may be effective when other methods, including evaporative cooling
techniques and iced gastric lavage, fail [PMID 2803356].
280
Iced urinary bladder lavage only
removed a trivial amount of heat in one study [PMID 9366461].
281
Recent animal studies suggest
that flushing of the nasal cavities with cooled gas (e.g., cooled nasal air) may protect the brain
against hyperthermal damage [PMID 12018975].
282
3) Cooling blood directly by removal, cooling, and re-introduction of blood
Advanced techniques such as this require specialized equipment. For example, successful
cooling of victims (resistant to other methods of rapid cooling) using cold hemodialysis (initially
86° F or 30° C) with cold continuous hemodiafiltration has been reported [PMID 16202019].
283
4) Medications
No medication has been shown to decrease core temperature. Dantrolene sodium did not
prove beneficial to patients with heatstroke in a randomized, double-blind, placebo-controlled
trial [
PMID 1989755].
284
However, research suggests dantrolene (a direct-acting skeletal muscle
relaxant) may lead to attenuated heat production and peripheral vascular relaxation [PMID
10519477].
285
C4.1.2. Cardiovascular Support
Preliminary work in animals suggests that maintenance of mean arterial pressure may be
important in the treatment of heat stroke [
PMID 11508869].
286
IV hydration should be done with
caution to avoid shifts of osmolality which may lead to cerebral edema and central pontine
myelinosis if done too rapidly [PMID 9267966].
287
Correction of reduced antithrombin III levels
to supranormal by therapeutic administration of antithrombin III concentrate and steroids in
disseminated intravascular coagulation of heat stroke has been reported [
PMID 12168565].
288
Treatment of heat stroke-associated conditions (DIC, rhabdomyolysis, arrhythmias, hypotension,
shock, ARDS, renal failure, liver failure, electrolyte abnormalities) may be required (including
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
37
the use of aggressive techniques such as mechanical ventilation, blood purification therapy
[PMID 10229168],
289
etc.)
C4.1.3. Concomitant Therapy
Heat stroke has been reported to be a risk factor for the development of disseminated
zygomycosis (one case of paranasal and GI zygomycosis in which Rhizopus schipperae was
cultured [PMID 10405417]).
290
Mechanisms regulating body heat may remain disturbed for days
following early treatment and apparent stabilization, mandating continued hospitalization [PMID
10959266].
291
After recovery, re-exposure to heat stress conditions must be done with caution.
Gradual acclimatization may eventually be successful, allowing the victim to be re-exposed
safely to heat stress conditions [PMID 2406545].
292
C4.2. Treatment of Heat Stroke - Clinical
C4.2.1. Preliminary Studies and Procedures
Treatment of heat stroke in the field should include immediate attempts to lower body
temperature to 101
o
F (38.3
o
C). The victim’s clothes should be removed. If there is a source of
cool water nearby, the victim should be immersed in it. Otherwise, water should be sprinkled
over the victim and evaporation hastened by fanning. Attendants should rub the victim's
extremities and trunk briskly to increase circulation to the skin. The victim should be transported
as soon as possible to a facility properly equipped to perform definitive treatment, with
paramedic-level attendant or higher if available [Noltkamper].
293
. During transportation, cooling
efforts should be continued by permitting passage of air currents through the open door of the
field ambulance or helicopter.
Rectal temperature should be obtained on presentation of the victim to the medical
facility. Laboratory studies should include a complete blood count (including hemoglobin,
hematocrit, white blood count, and platelet count), PT/PTT, electrolytes (sodium, potassium,
bicarbonate, chloride), blood urea nitrogen, creatinine, glucose, hepatic transaminases (AST,
ALT), lactate dehydrogenase, creatinine kinase, and urinalysis. A full (12 lead) EKG and urine
drug screen should be obtained. A chest x-ray and arterial blood gas (ABG) should be done if
indicated. If ABGs are deemed necessary, the lab should be informed of the patient's body
temperature in order to make corrections in determining the results. As in any patient with
altered mental status and fever, a toxicologic screen and lumbar puncture may be indicated if the
etiology is unclear. As cocaine may cause hyperthermia, special consideration should be given to
assessing for cocaine. Blood osmolality, myoglobin, and urine myoglobin may be useful in
patient management, although they may not be readily available. Calcium, magnesium,
phosphorous, uric acid, protein, albumin, and lactic acid levels may be helpful in managing
severe cases, and are recommended if there is suspicion of internal organ damage.
If heat stroke (or impending heat stroke) is a diagnostic possibility, continuous body core
temperature readings should be taken via esophageal thermometer. If that is not available, rectal
temperatures should be measured frequently, at least every 15 minutes. In addition, the victim’s
mental status should be checked frequently, as should blood pressure and urine output and color.
Definitive medical treatment should begin with general supportive therapy, including
oxygen (by face mask or nasal cannula) or endotracheal intubation, as increased tissue oxygen
requirements induced by hyperthermia are expected [
PMID 3063579].
294
Endotracheal
intubation should be used in any patient with a reduced level of consciousness and in any heat
stroke patient that has been sedated. IV fluid administration should be started, with the notation
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
38
that dehydration and volume depletion may be limited in heat stroke [PMID 1852063].
295
NS or
LR at 250 ml/hour may be required; however, heat stroke victims may be especially prone to
congestive cardiac failure and pulmonary edema from excessive fluid administration [PMID
1852063].
296
An NG tube should be placed to prevent aspiration in non-alert patients and for
potential gastric lavage or administration of medications. A foley catheter should be placed and
urine output monitored.
Exercise in heat stress conditions may cause hypoglycemia [
PMID 1602940],
297
[PMID
2132167],
298
and hypoglycemia in heat stroke has been reported [PMID 3398504].
299
(However,
hypoglycemia in heat stroke is reported to be rare by other authors [
PMID 12075060].)
300
It is
recommended that hypoglycemia is confirmed (for example, fingerstick blood glucose
determination) prior to using IV fluids contain glucose.
If there is inadequate urine output after continued IV fluid resuscitation, osmotic diuretics
(e.g., mannitol) may be considered. However, central line or Swan-Ganz monitoring may be
desirable to ensure appropriate fluid administration [PMID 1852063].
301
Whether hypotensive
patients who do not respond to saline should receive inotropic support is uncertain. Use of
norepinephrine, if deemed necessary for hemodynamic control, probably should be avoided until
after successful cooling has been accomplished. Increases in both norepinephrine and
epinephrine have been found in patients with heat stroke, indicating activation of the sympatho-
adrenal system, and researchers suggested that the alpha-mediated effect of catecholamines may
be important in impairing heat dissipation and may contribute to the pathogenesis of heat stroke
[
PMID 2499843].
302
Additionally, experiments in rats demonstrated increased extracellular
concentrations of dopamine, serotonin or norepinephrine in the hypothalamus and other brain
regions during heatstroke-induced cerebral ischemia and neuronal damage; heatstroke-induced
cerebral ischemia and neuronal damage were attenuated and survival increased by depletion of
brain dopamine or serotonin [PMID 9100936].
303
C4.2.1.1.1. Shivering
Overcooling may result in shivering [PMID 1608386].
304
Shivering is associated with
increased involuntary muscular activity (which may accentuate tissue hypoxia and lactic acid
acidosis). If simple warming measures fail to control shivering, IV benzodiazepines (such as
diazepam 10 mg) may be helpful. Benzodiazepines may also be given for seizures or severe
cramping [
PMID 9694424],
305
[PMID 12075060].
306
Antipyretic agents are not indicated
(although aspirin may have some efficacy in treatment of platelet aggregation abnormalities in
heat stroke [PMID 231070]).
307
C4.2.1.1.2. Electrolyte Abnormalities
In both classical and exertional heatstroke and in various animal models of human heat
injury, clinical manifestations have included observations of normokalemia, hyperkalemia, and
hypokalemia [
PMID 11990141].
308
(Some authors report severe hyperkalemia to be common in
patients with exertional heat stroke but uncommon in those with classical heat stroke [PMID
7078400],
309
while other recent reports found hypokalemia or normokalemia instead of
hyperkalemia [PMID 7644768].)
310
C4.2.1.1.3. Rhabdomyolysis
Rhabdomyolysis may be recognized by discoloration of urine, and should be suspected in
all cases of heat stroke. It may cause release of creatinine kinase and myoglobin into the vascular
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
39
system, and may be associated with elevated uric acid, phosphate, and potassium levels (as well
creatinine kinase and myoglobin). Rhabdomyolysis may lead to renal failure due to renal
vasoconstriction, tubular damage caused by oxidant injury, and possibly tubular obstruction
[
PMID 11430535].
311
Urine alkalinization and increasing urine flow by osmotic diuretics such as
mannitol may help minimize renal injury. Once renal injury has been sustained, hemodialysis
may relieve plasma myoglobin load as well as biochemical abnormalities [
PMID 11417950].
312
C4.2.1.1.4. Renal Injury
Acute renal injury (acute renal failure, renal tubular necrosis) is common in exertional
heat stroke, rhabdomyolysis being the major mechanism among multifactorial causes of renal
failure [PMID 7644768].
313
Uric acid may play a role in heat-related renal injury [PMID
6611841].
314
Continuous venovenous hemofiltration has been reported to be a good alternative to
dialysis in hemodynamically unstable patients [PMID 7644768].
315
Core body temperature
should be monitored closely until stable.
C4.2.1.1.5. Other Associated Injury
Liver involvement is common in heat stroke, usually manifested by increased serum
levels of liver enzymes, and acute liver failure has been reported [PMID 15105986].
316
Extensive
hepatocellular damage requiring liver transplant has been reported [PMID 15838872],
317
as has
spontaneous recovery of a case that initially was thought to require liver transplantation [PMID
15105986].
318
Lower leg compartment syndrome has rarely been seen as a complication of or in
conjunction with heat stroke [Noltkamper],
319
especially in sickle trait [PMID 8677839];
320
health care providers should be aware that compartment syndrome may itself cause
rhabdomyolysis [PMID 7569117].
321
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
40
Chapter 5:
C5. Follow-up of Heat Stress Injuries
After a heat stress injury, victims are less resistant to heat stress injuries. They are also
40% more likely to require hospitalization (although not necessarily related to heat injury) during
the next four years, with that elevated rate of hospitalization decreasing over time [PMID
11528330].
322
Important aspects of post-incident care include adequate medical follow-up,
careful re-exposure (or avoidance of re-exposure) to future heat stress conditions, reporting, and
prevention of other heat stress injuries in the involved population.
C5.1. Monitoring Health after Heat Stroke Recovery
It is recommended that all heat stroke-related abnormal studies be followed to normal
after recovery. In addition, at least one careful neurological examination is recommended at 3
months after injury. Any abnormalities should be thoroughly investigated. MRI and/or
neuropsychiatric testing may be indicated.
C5.2. Care of Residual Disability or Deficits after Heat Stroke
In one series of classic heat stroke victims, moderate to severe functional impairment was
noted in 33% of patients at hospital discharge, and one year later no patient had improved
functional status [PMID 9696724].
323
One series of young heat stroke victims concluded that
prominent neurological or behavioral sequelae in heat stroke victims are rare [PMID
8372119].
324
However, cases of cerebellar atrophy related to heat stroke have been reported, in
which the atrophy was first noted on MRI studies 10 weeks to months after injury, and which
progressed during one or more years follow-up [PMID 9106293],
325
[PMID 7788975],
326
[PMID
7575855].
327
C5.3. Re-Exposure to Heat
C5.3.1. Minor Injuries
Most victims of minor heat stress injuries can safely be re-exposed to heat stress
conditions 24 hours or less after complete recovery. Once miliaria has resolved, victims may be
re-exposed to heat stress. Victims with hyperthermia (elevated core body temperature without
other apparent injury) should wait until after core body temperature has been documented to be
less than 99°F (37.2°C) prior to re-exposure to heat stress conditions. Heat syncope victims
should wait until core body temperature is documented to be normal prior to re-exposure to heat.
Those who have experienced heat tetany may resume acclimatization after the acute condition
resolves. Persons with heat edema may continue acclimatization. If edema becomes severe, they
may require more gradual acclimatization. Victims with heat cramps should wait 24 hours after
cramps have resolved and salt replenishment is administered (whichever is later) prior to re-
exposure to heat stress.
C5.3.2. Major Injuries
C5.3.2.1.1. Heat Exhaustion
Those who have suffered heat exhaustion should wait at least 48 hours after core body
temperature, serum electrolyte values, and all heat stress-related studies have been documented
as normal prior to re-exposure to heat stress. Clinical judgment by the health care provider may
prolong this period on an individual basis.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
41
C5.3.2.1.2. Heat Stroke
Recovered heat stroke victims must be recognized as having survived a life-threatening
medical emergency. Re-exposure to heat must be on a case-by-case basis, according to the
clinical judgment of a physician. At a minimum, it is recommended that heat stroke survivors
avoid all heat stress for 2 weeks after hospital discharge and stabilization and normalization of
all heat stroke-related studies. Access to air-conditioning as necessary if possible is
recommended. After 2 weeks, brief excursions into heat stress conditions may be allowed, as
long as there is only minimal physical exertion and prompt re-entry into air-conditioning is
available (for example, short walks).
Attempts at acclimatization after heat stroke should be delayed until at least 40 days after
complete recovery (based on a series in which mean time to acclimatization was 61 days) [PMID
2406545].
328
Some victims will not successfully acclimatize until months later, if at all [PMID
2406545].
329
Some researchers have recommended testing 8 to 12 weeks after heat stroke to
detect possible inability to cope with heat stress adequately [
PMID 2406544].
330
C5.4. Reporting
All Navy heat stress-related injuries should be reported through the Naval Disease
Reporting System. A simultaneous report to the Naval Safety Center should be made using the
Web Enabled Safety System (WESS). Marine Corps heat injuries should be reported in
accordance with MCO P5102.1A (which prescribes the mandatory use of electronic mishap
reporting of all Marine Corps ground mishaps to the Marine Corps database maintained at the
Naval Safety Center) and BUMEDINST 6220.12A (which stipulates Naval Disease Reporting
System electronic report, or written, fax, e-mail or phone report to the cognizant
NAVENPVNTMEDU).
331
C5.5. Prevention of Further Heat Stress Injuries in the Population
When a heat stress injury is recognized, steps should be taken to prevent others in the involved
population from heat stress injury. The victim may serve as a sentinel event, alerting health care
workers, safety, and supervisors to the existence of a heat-related health risk. Training on heat
stress injuries may be appropriate (see OPNAV 5100.23 series Chapter 29).
332
A check of
WBGT equipment should be done, if it is possible that faulty equipment may have contributed to
the heat stress injury. Adequacy of water supply, cooling facilities (HVAC system, if present),
and clothing should be verified. With appropriate measures, most heat stress-related injuries can
be prevented.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
42
Chapter 6:
C6. Criteria for the Diagnosis of Heat Stroke
The following table is set forth for use in non-emergent care of severe heat stress injury
victims. For diagnostic criteria for use in acute care situations, see
Figure 5 (page 26).
Abnormality Criteria Notations Points
105° F or higher
(40.6° C)
•
Taken by any means of
instrumentation (i.e., not only with
hand on forehead)
•
No known underlying condition to
explain the high body temperature
(for example, fever due to infection)
4
103° F to 104.9° F
(39.4° C to 40.5° C)
•
Taken by any means of
instrumentation (i.e., not only with
hand on forehead)
•
No known underlying condition to
explain the high body temperature
(for example, fever due to infection)
2
101° F or higher
(38.4° C) after
cooling
•
105° F or higher (40.6° C) suspected
from history but not documented
•
No known underlying condition to
explain the high body temperature
(for example, fever due to infection)
2
Temperature
elevation
Undocumented
•
Suspected to have been 105° F or
higher (40.6° C) based on history
1
•
Confusion,
extreme and
persistent
•
Delirium
•
Seizures
•
Coma
•
Not due to other causes (no CNS
trauma, no toxicant, no CNS
infection)
4
Disordered
mentation
•
Mild confusion
•
Disoriented
•
Does not clear or resolve
immediately
2
Cardio-
vascular
abnormalities
•
Arrhythmias
•
Hypotension
•
Ischemia
•
Pulmonary edema
•
Not present prior to exposure to heat
stress exposure
2
D
isseminated
intravascular
coagulopathy (DIC)
•
Abnormal clotting studies
•
Hemorrhage (skin, gastrointestinal,
genitourinary)
2
Coagulation
abnormalities
•
PT or PTT ≥ twice
normal
•
Platelets <
100,000
•
Without other known explanation
1
Re
q
uired for dia
g
nosis of heat stroke
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
43
Rhabdomyo-
lysis
•
Myoglobinuria
(positive urine
myoglobin test)
•
Elevated serum
myoglobin (radio-
immunoassay >
100)
•
Without other explanation (crush
injury, overexertion, alcohol abuse,
medicines, toxicants)
•
If serum myoglobin, without other
explanation of elevated serum
myoglobin (such as myocardial
injury)
2
Sweating
abnormalities
Cessation of
sweating
•
In spite of exposure to heat stress
conditions
1
Respiratory
distress
Adult respiratory
distress syndrome
(ARDS)
•
Without other explanation
2
Shock BP < 90/60
•
With evidence of inadequate organ
perfusion
•
Without other explanation
2
Hypernatremia
•
Sodium > 150
1
Hypophosphatemia
•
Inorganic phosphorus < 2.5 mg/dL
2
Hypokalemia
•
Potassium < 3.1
1
Blood
chemistry
abnormalities
Hyperkalemia
•
Potassium > 5.5
1
Total required for heat stroke diagnosis
• Must be 6 or more
• Must include points from both temperature and CNS categories
• Treatment for heat stroke should not be delayed until a definite diagnosis of heat
stroke is made using the above criteria (which may take days to develop). Instead,
Figure 5 - Acute Heat Exposed Patient Diagnostic Flow Chart, page 26, should be
used.
Table 10 - Diagnostic Criteria for Heat Stroke
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
44
Chapter 7:
C7. Physiology of Cold Stress
C7.1. Introduction
In contrast to heat stress, cold stress presents challenges to the body in retaining heat
produced by metabolism. Air temperatures 88° F (31.1° C) and lower may represent cold stress
conditions to healthy people (for example, in newborns 2 to 10 days old) [PMID: 3970567],
333
and temperatures below 95° F (35° C) may pose a risk of cold stress injury to individuals without
insulation or without functioning thermoregulatory mechanisms [Currier].
334
Overall death rates from all causes increase during winter. In addition to hypothermia,
cold temperature is associated with excess mortality from ischemic heart disease and
cerebrovascular disease [CDC].
335
Cold temperature also can lower the immune system's
resistance to respiratory infection, causing an increase in respiratory disease mortality [CDC]
336
[PMID: 9149695].
337
Hypothermia decreases performance [PMID: 16538942],
338
increases the
risk of bleeding [PMID: 15211129],
339
and is an independent risk factor of mortality in trauma
patients [PMID: 16385283].
340
Hypothermia may also alter the response to certain medications
(e.g., increased rather than decreased blood pressure from thiopental) [PMID: 17023288].
341
C7.1.1. Heat Transfer or Loss from the Human Body
The human body is constantly producing heat by metabolism. Heat is transferred from the
human body by radiation (generally to massive objects colder than the body), conduction (by
touching cold surfaces or liquids), convection (by air colder than 95° F or 35° C passing over the
body, and by exhaled breath that has been warmed to body temperature leaving the body), and
evaporation (by sweat, water, or other liquid vaporizing from the body surface, absorbing heat as
it does so). Clothing, personal protective equipment, and fat serve as insulation against heat loss
from the body. Activity and certain conditions (for example, fever from infection) increase
metabolism and heat production.
C7.1.2. Cold Stress, Cold Strain, and Cold Injury
When the net heat balance at a given activity level with typical clothing would result in
heat loss unless the body compensates by thermoregulatory mechanisms, cold stress conditions
are said to exist. When cold stress conditions are such that normal body temperature can no
longer be maintained (either generally—throughout the body—or “locally”—that is, at specific
body parts, such as fingers or toes), the body may be said to be undergoing cold strain. Cold
strain, if of sufficient degree or duration, may result in cold injury (either to the whole body—
e.g., hypothermia, or to areas of the body—e.g., frostbite).
C7.2. Environmental Cold Stress Factors
C7.2.1. Temperature and Wind
The primary factors in thermal stress are the temperature and air movement of the
immediate environment. The higher the air (wind) speed, the greater the cooling effect from
convection and evaporation (termed windchill). However, as wind speed increases, friction from
wind begins to generate enough heat to diminish cooling efficiency. For example, 20° F (-6.7° C)
in calm or no air movement conditions (“calm temperature”) becomes 13° F (–10.6° C) windchill
(see below) at 5 miles per hour (mph) wind speed, 4° F (–15.6° C) wind chill at 20 mph, and
-4° F (–20° C) at 60 mph [
NWS].
342
(The first 5 mph increase in wind speed drops the wind chill
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
45
temperature 7° F, but the last 40 mph increase in wind speed drops the wind chill temperature
only another 8° F.)
C7.2.2. Windchill Temperature Index
The Windchill Temperature Index is a calculation of the cooling effect on the body of
cold weather conditions, taking into account temperature and wind speed.
1
The National Weather
Service has recently implemented an updated equation, and future adjustments are expected to
take into account sunny and cloudy sky conditions [NWS].
343
The formula used by the US and
Canadian national weather services as of November 1, 2001 is:
Windchill (°F) = 35.74 + 0.6215T - 35.75(V
0.16
) + 0.4275T(V
0.16
)
where:
V = the wind speed value in mph and
T = the temperature in °F
344
No adjustments are made for sky conditions; a clear night sky is assumed [NWS].
345
Windchill index calculators are available on the Internet.
346
Note: Frostbite occurs in 15 minutes or less at windchill values of -18° F (-27.8° C) or
lower [NWS].
347
C7.2.3. Humidity and Moisture
Humidity affects environmental cold stress by affecting how quickly evaporation (for
example, of sweat) from the skin takes place.
2
Under dry conditions, a person with moist or wet
skin who finishes exercising will lose heat rapidly. While sweat that runs or drips off does not
facilitate significant heat removal in a hot environment, soaked skin or clothing may increase
conductive and convective heat loss in a cold environment, especially if there is contact with
cold surfaces or cold moving air.
C7.2.4. Immersion
Immersion in cold water presents special challenges to personnel. Even though seawater
does not normally get below 28.6° F (-1.9° C) without freezing, water absorbs a larger amount of
heat than air after penetrating clothing; i.e., water has a relatively high sensible heat, which is
“the amount of heat that, when absorbed by a substance, causes a rise in temperature”
[Stedman’s].
348
The cold stress of immersion in 30° F (-1.1° C) seawater may be much greater
than that of standing on dry land at the same temperature.
C7.2.4.1. Diving Reflex
Immersion triggers the diving reflex (bradycardia response) [
PMID: 11816961].
349
The
colder the water, the more marked the bradycardia (a 9% decrease in heart rate with facial
immersion at 98.6° F or 37° C and a 29% decrease in heart rate at 37.4° F or 3° C) [
York].
350
1
The term “wind chill factor” is often used to refer to the wind chill temperature index, although it may be used to
refer to the significance of wind as a contributor to the effective temperature, or (perhaps more properly) to the
calculation itself.
2
The quantity of heat absorbed by water changing to steam is the “latent heat” or “heat of transformation.”
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
46
C7.2.4.2. Fluid shifts in Cold Water
Vascular fluid shifts, body cooling, and diuresis are all greater in cold water than in cold
air [PMID: 3629738].
351
The percent reduction in plasma volume from cold exposure is
significantly larger in cold water (-17%) than in cold air (-12%) [
PMID: 3629738].
352
C7.2.4.3. Performance in Cold Water
Immersion in cold water impairs swimming performance (at 64° F or 18° C, and even
more at 50° F or 10° C), which, with initial cardio-respiratory responses to immersion, probably
is the major danger to cold-water immersion victims [PMID: 10466663].
353
Protective effects of
increased body fat against cold stress, although significant on dry land [
PMID: 6735815]
354
and
during immersion [
PMID: 11043627],
355
are minimal compared to the benefit of a dry suit
during cold-water immersion [PMID: 2803162].
356
C7.2.4.4. Swimming Induced Pulmonary Edema (SIPE)
SIPE, also in the literature termed “cold-induced pulmonary edema,” “scuba induced
pulmonary edema” and “pulmonary oedema induced by strenuous swimming (SIPO)” [PMID:
10854620],
357
has been associated with swimming and diving. Previously thought to be a cold-
water phenomenon, recently (1997) it has been reported in warm water [PMID: 9068153],
358
[PMID: 11728772].
359
Symptoms include dyspnea, cough, sputum production, hypoxemia
(saturation 85 to 90%), hemoptysis (in about half of victims), weakness, chest discomfort,
orthopnea, wheezing, and dizziness. Physical examination may reveal rales. Chest X-ray is
usually normal or with evidence of pulmonary edema, and spirometry may show a restrictive
pattern. Recurrence is not uncommon (approximately 20% experience recurrence) [PMID:
10854620],
360
[PMID: 9068153].
361
Treatment is usually conservative, aimed primarily at
resolution of pulmonary edema. Resolution of symptoms is usually within 1 or 2 days, although
fatal outcomes have been reported [PMID: 15796313].
362
C7.2.4.5. Awareness of Cold Strain in Cold Water
Personnel immersed in cold water cannot reliably assess how cold they are [PMID:
2803163].
363
With immersion in mildly cool water, stability of the temperature of cutaneous
receptors may lead to hypothermia without personnel being aware of their condition [PMID:
3795105].
364
C7.2.4.6. Cardiac Output in Cold Water
Head-out water immersion at thermo-neutral temperature increases cardiac output by
increasing stroke volume; this is greater in cool (86°F or 30° C) water. Also, total peripheral
resistance decreases (32% in one study) in cool water. Thus, cardiac output at a given work load
is significantly higher in water than in air [PMID: 10675972].
365
C7.2.4.7. Survival Times in Cold Water
Survival times in cold water have been studied. Cold-water immersion of either men or
women (at 32° F or 0° C) initially increases the ventilation rate (more than 4 times baseline for
the first 2 minutes of immersion). After 10 minutes of immersion, mean skin temperature falls to
41° F (5° C), and rectal cooling rate is 10.8° F (6° C) per hour. After 20 minutes of immersion,
maximum shivering metabolism peaks at nearly 4 times pre-immersion [
PMID: 6721816].
366
Swimming increases heat production to 2.5 times that of holding still (simply floating) in cold
water (at 50.9° F or 10.5° C water temperature), but also increases the cooling rate 35%. A
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
47
prediction equation for survival time of persons accidentally immersed in cold water (32° F to
71.6° F, or 0° C to 22° C) is as follows [PMID: 1139445].
367
Survival Time = 15 + 7.2/(0.0785 – (0.0034 x water temperature in °C)).
Survival time may be shorter in very cold water (e.g., one hour at 32° F or 0° C) [
PMID:
6721816],
368
and in rough seas [PMID: 3606516].
369
Actual survival without flotation devices
may be much less (e.g., 2 to 5 minutes in seawater at 29° F or –1.67° C) [Navy].
370
In falls through thin ice, the greatest risk comes from drowning (both to the individual
and to the rescuers). The victim should control their breathing, make their way to the side where
they fell in (where the ice is stronger), attempt to extricate themselves (using implements such as
ski poles via the high dagger method, if available), and hold on to the side, perhaps even freezing
to the ice with their sleeves. Rescuers should plan the rescue properly, not rushing to the edge or
jumping in to save the victim and perishing themselves: there is some time before hypothermia
will become deadly.
371
Figure 6 - Survival Time in Cold Water (estimated)
C7.2.4.8. Diving Suits
A study of cold-water exposure in diving suits showed that
• “Dry suits” provide better protection than "wet suits;"
• In rough seas, tight-fitting wet suits provide better protection than loose-fitting wet suits;
Survival Time in Cold Water
Assuming Use of Flotation Device to Prevent Drowning
0
100
200
300
400
500
600
700
800
0 5 10 15 20 25
Water Temperature
(degrees Fahrenheit) (degrees Celsius)
Minutes
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
48
• Cold-water immersion in rough seas causes greater body core temperature decrease than
in calm seas;
• Accidental immersion in rough seas may be associated with significantly lower survival
times than would be estimated from calm-water studies [
PMID: 3606516].
372
C7.2.5. Elevation (Altitude)
Altitude may accentuate certain responses to cold stress. The respiratory responses during
acute cold exposure (see below) are similar to those of initial altitude responses [PMID:
8468097].
373
It is felt by some that cold can predispose individuals to high altitude pulmonary
edema [PMID: 9152300].
374,375
Acclimatization to cold exposure at higher altitudes may appear to occur faster than it
really does, as heart rate and blood pressure decreases may occur from a transient reduction in
parasympathetic and sympathetic activity during initial stepwise exposure to high altitude
[
PMID: 11903133].
376
Frostbite is common in mountain climbers; one study of self-reported history of frostbite
injury showed a mean incidence of 366/1000 population per year, significantly related to lack of
proper equipment and to not having a guide [
PMID: 16306495].
377
C7.2.6. Contact and Handling of Cold Objects
Contact with cold objects (metal, ice, cold water, etc.) generally presents cold stress
challenges only locally, unless there is a large area of skin contacting a very large object.
Sensation on contact with very cold objects (-20° F or –28.9° C) includes tingling, pain, and
burning (sometimes with almost no sensation of cold) [Daniels].
378
One experimental investigation concluded that metal surfaces in contact with bare hands
should not be below 39.2° F (4° C) surface temperature, and that lower temperatures require
insulating material or the wearing of protective gloves [PMID: 7957157].
379
Contact pressure,
contact material mass, surface temperature, and whole body thermal balance all were found to
significantly impact contact skin temperature change with time. Of special concern is that in
persons handling cold metal objects with their fingers, pain and temperature sensation do not
correlate well with skin temperature or change in temperature [
PMID: 8184801].
380
Also, once
skin temperature falls below 46.4° F (8° C), tactile sensations do not function and warn (e.g., of
freezing conditions and impending frostbite); hence, some investigators have chosen to use that
temperature as the limit for frostbite risk [PMID: 8049001].
381
Some clinicians feel that allowing
limited ungloved handling of metal objects may be safe for experienced personnel.
382
In addition to discomfort and decreased sensation on cold exposure of the skin, hand
performance is substantially reduced at skin temperatures below 59° F (15° C) (see below,
Dexterity when Handling Cold Objects) [PMID: 8049001].
383
Local hypothermia (cooling the
forearm to 86° F or 30° C and to 82.4° F or 28° C) was found to increase local bleeding time but
did not affect bleeding time at other parts of the body [
PMID: 17096671].
384
C7.2.6.1. Time to Reach Contact Temperature
In examining the time it takes to cool the hand when gripping a cold object, researchers
found that women were found to reach a “contact temperature” (i.e., the temperature of the palm
of the hand—in the study, 59° F or 15° C) significantly faster than men (in approximately only
70% of the time it takes men’s palms to reach the same temperature) [
PMID: 12074025].
385
Interestingly, the same study found that time to reach a contact temperature was actually longer
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
49
when subjects were standing in a cold room, rather than standing in a warm room and inserting
their hands into a cold box [PMID: 12074025].
386
The little finger is the limiting factor in
exposure of the hand to cold air, as it is particularly vulnerable to rapid cooling [Daniels].
387
C7.2.6.2. Dexterity when Handling Cold Objects
Exposure to the cold may negatively influence manual dexterity [
PMID: 12074025].
388
Hand skin temperature, rather than body surface temperature, is the critical factor; when hand
skin temperature is 55° F (12.8° C) or lower, manual performance is impaired [PMID:
5905109].
389
Manual performance (finger dexterity in knot tying) is further decreased a skin
temperature falls further (e.g., to 45° F or 7.2° C), and at slower rates of cooling (generally
associated with the fingers being exposed for longer times to less-severe cold) [PMID:
13810475].
390
Military researchers have noted that insulating metal equipment (e.g., with foamed
plastic) in the cold is more feasible than trying to maintain manual dexterity by insulating the
hand, and have suggested “it is probably impossible to design a glove or mitten with adequate
insulation which will permit all fine manipulations to be performed as quickly and as accurately
as they can be done with the bare hand” [Daniels].
391
C7.2.6.3. Freezing to Cold Objects
Touching very cold objects (such as touching cold metal with the tongue or fingers) is
known to cause the body part to stick to the object. Freezing to cold metal has been studied and
found to occur only when an “ice bridge” is formed from free water on the surface of the body
part or object [Daniels].
392
C7.2.7. Ultraviolet Light
Exposure to cold may also be accompanied by excessive ultraviolet light exposure
(including ultraviolet light reflected off of snow or ice—for example, in the arctic) [PMID:
2021394].
393
Thus, when protecting against cold exposure, it may be appropriate to also consider
eye and skin protection often associated with warm weather (sunglasses and sunscreen lotion).
C7.3. Individual Cold Stress Factors
C7.3.1. Body Mass and Fat
Individuals with higher body mass and more body fat can better tolerate cold stress
exposure [
PMID: 984737].
394
C7.3.2. Gender
Males tend to use carbohydrates and fats equally in their metabolic response to cold
stress; females may use much more fats than carbohydrates [
PMID: 10198139],
395
but not all
studies support that finding [
PMID: 3780704].
396
At least one review has concluded that
individual body size, physical fitness, and state of acclimatization play for more important roles
than gender in determining human thermal responses [PMID: 750842].
397
C7.3.3. Age
In a cold environment, children have lower skin temperatures, reflecting greater
vasoconstriction [PMID: 9587181].
398
Elderly (65 to 89 years of age) subjects exhibited less heat
production, attenuated skin vasoconstrictor response, and lower core temperature after exposure
to mild cold stress [PMID: 17197640].
399
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
50
C7.3.4. Race and/or Ancestral Geographic Location
In one study, high altitude (11,500 feet or 3500 meters above sea level) natives
maintained significantly higher oral temperature, mean body temperature, and skin temperature
during sea level cold stress; they shivered much less, and showed higher peripheral blood flow
than “lowlanders;” however, there was no difference found in the rise in oxygen consumption in
cold stress [PMID: 464958].
400
Different types of general cold adaptation have been described in
different people groups, including metabolic adaptation (Alacaluf Indians, Arctic Indians),
insulative adaptation (coastal Aborigines of tropical northern Australia), hypothermic adaptation
(bushmen of the Kalahari desert, Peruvian Indians) and insulative hypothermic adaptation
(Central Australian Aborigines, nomadic Lapps, Korean and Japanese diving women) [PMID:
1483765].
401
Whether genetics or climate characteristics are responsible in each case is not
established; acclimatization (see below) to cold stress is possible in men from tropical climates
as well as men from temperate zones [PMID: 1297856].
402
C7.3.4.1. Metabolic Adaptation
Indigenous circumpolar people groups have systematic and statistically significant
elevations in basal metabolic rate (BMR) ranging from 7% to 19% above predicted values for
indigenous men and from 3% to 17% for indigenous women [
PMID: 12203815].
403
This is
considered a metabolic adaptation to cold stress (also see Metabolism, below).
C7.3.4.2. Insulative Adaptation
A group of acclimatized cross-country skiers was found to have lower skin temperatures
after exposure to cold stress; metabolic heat production was not increased [PMID: 1555569].
404
This is an insulative adaptation to cold stress.
C7.3.4.3. Hypothermic Adaptation
A group of study subjects exposed to cold for 10 days showed an increase in the delay
before the onset of shivering and a decrease in the core temperature at the onset of shivering
[PMID: 11507988],
405
termed a hypothermic adaptation.
C7.3.5. Alcohol
Alcohol (ethanol) can cause cutaneous capillary dilation, which in turn may
inappropriately increase cutaneous blood flow during cold exposure. Skin temperature fall will
be blunted, while core temperature will fall more quickly. Thus, alcohol may diminish
thermoregulatory responses associated with acclimatization: when rectal and skin temperatures
decrease simultaneously, thermoregulation is greater than when rectal temperature alone changes
[PMID: 8900834].
406
A recent case report noted that severe ethanol poisoning, in the absence of
any other contributing factors, may explain hypothermia [
PMID: 17251602].
407
However,
studies have concluded that in cold exposure, moderate alcohol consumption predisposes
individuals to hypothermia more by behavioral factors than via impaired thermoregulation
[
PMID: 497899]
408
[PMID: 8897037].
409
C7.3.6. Hydration
Cold exposure may lead to significant dehydration (via cold diuresis, high energy
expenditures, and poor access to water) [PMID: 7639888].
410
Urine specific gravity is often used
to monitor hydration status in field settings. However, one study of cold exposure found no
significant correlation between changes in total body water and urine specific gravity or other
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
51
typical urinary indicators of dehydration [PMID: 7639888].
411
In addition, a study of Marines in
a cold environment found that dehydration might not be readily noticeable in the field, due to
maintenance of circulating volume at the expense of both intracellular and extracellular water
[
PMID: 3116457].
412
The same study found that inadequate drinking water availability was
associated with inadequate nutritional intake (troops preferred to go hungry) [
PMID:
3116457].
413
C7.3.7. Central Nervous System (CNS) Abnormalities
CNS abnormalities involving the corpus callosum (including agenesis of the corpus
callosum, multiple sclerosis, and previous head injury) have been associated with abnormal body
temperature regulation in what has been termed “spontaneous hypothermia” or Shapiro's
syndrome [PMID: 16459729,
414
PMID: 17250734].
415
The disorder has an unpredictable course,
generally with long periods of remission [PMID: 15990200].
416
C7.3.8. Heat Debt
Heat debt refers to the net amount of heat lost to the environment that would be necessary
to return the entire body to normal temperature in thermo-neutral conditions. The term is often
used in studies of the effects of cold stress exposure, but is generally not of use in clinical
practice.
C7.4. Compensation for Cold Environments
C7.4.1. Functioning in Cold Environments
Moderate cold exposure (even that does not produce core hypothermia) can impair
performance of complex cognitive tasks [PMID: 2818396].
417
Mechanisms to compensate with
cold environmental temperatures include behavior changes (voluntary muscular activity and
exercise, staying indoors, wearing warm clothing, growing—or allowing to grow longer—a
beard and/or long hair) and physiological responses. Physiological responses to cold stress
include increasing body fat (which acts as insulation and as an energy reserve for increased
metabolic needs), increased appetite (related to increased body fat), increased (or decreased)
metabolism, increased activity, decreased cutaneous blood flow (resulting in cool skin, which
may appear pale, mottled, or blue), shunting of blood from skin and extremities (to decrease
cutaneous loss of heat, but which may increase likelihood of Chilblains and frostbite), and
shivering. Certain individuals demonstrate a response termed paradoxical undressing (a
pathologic response occasionally seen in alcoholics exposed to cold stress [
PMID: 541627]
418
[
PMID: 2036058]).
419
Infants, but not adults, can also increase thermogenesis by the metabolism
of brown fat [
PMID: 9180091].
420
Manual dexterity is decreased after cold exposure [PMID: 11374119].
421
Maximum grip
strength improves somewhat immediately following the application of cold and then declines
[PMID: 4083336].
422
Peripheral motor nerve conduction velocity has been found to decrease by
15 meters per second for every 18° F (10° C) fall in tissue temperature; at a tissue temperature of
46° F to 50° F (8-10° C), a complete nervous block was established [
PMID: 1115693].
423
Exposure to cold is frequently in high altitude environments. Prolonged high altitude
exposure is often accompanied by considerable weight loss, thought to be due to primary
anorexia, lack of comfort and palatable food, detraining, and possible direct effects of hypoxia
on protein metabolism [PMID: 1483750].
424
Absorption of protein and fat has not been shown to
be a factor, at least up to 5000 feet above sea level [PMID: 1490954].
425
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
52
C7.4.2. Metabolism
C7.4.2.1. Muscles
Lactate levels with work in cold exposure are generally higher than with work in milder
conditions; the time lag between production of lactate within the muscle and its release into the
venous circulation may be increased by cold exposure [PMID: 1925184].
426
C7.4.2.2. Body Fat
Significant inter-individual variation exists among persons exposed to cold stress in both
body temperatures and energy expenditures (adjusted for body composition) [PMID:
11934673].
427
Individuals with less body fat tend to expend more calories when exposed to cool
water [
PMID: 11990094].
428
Increased oxidation of carbohydrates and free fatty acids is a well-known phenomenon
during cold stress [PMID: 12079880].
429
Human studies have shown that cold exposure
increases lipid oxidation [PMID: 2233284].
430
Fat oxidation increases during shivering in
prolonged (105 to 388 minutes) immersion in cold water; plasma glucose increases, and is lower
during intense shivering than during moderate shivering [PMID: 12012076].
431
In one study,
during exercise for 90 minutes in cold air, fat oxidation was found to be diminished, thought by
researchers to reflect either a reduction in lipolysis and/or mobilization of free fatty acids or
impairment in the oxidative capacity of muscle [PMID: 11984294].
432
Free fatty acid levels are
not higher with exercise in cold air or water [PMID: 1925184].
433
Cold-induced vasoconstriction
of peripheral adipose tissue may account, in part, for the decrease in lipid mobilization [PMID:
1925184].
434
C7.4.2.3. Hormones
Plasma concentrations of epinephrine, insulin, cortisol, and growth hormone are
unaffected by cold exposure; norepinephrine increases about threefold [PMID: 12079880].
435
Decreased fertility has been noted with cold exposure, which is thought to change
metabolic fuel oxidation, affecting viscera and parts of the brain (the hindbrain in animals),
which in turn affect the activity of gonadotropin-releasing hormone neurons in the forebrain
[PMID: 8772468].
436
C7.4.2.4. Calories and Cold Exposure
C7.4.2.4.1. Caloric requirements
The change in core temperature that occurs as a result of exposure to cold air or water
affects all body systems [
PMID: 11816961].
437
The calorie requirements of adequately clothed
men living and working in a cold environment are not increased, except for the 2-5 percent
increase in metabolic rate due to effort required by heavy clothing [
PMID: 844611].
438
Exercising in cool water has not been found to increase energy expenditure and weight loss
(beyond the effect of exercising in general) [PMID: 7068314].
439
One investigation reported that during prolonged, low-intensity shivering, the energy for
heat production is from lipids (50%), carbohydrates (40%, with 30% from muscle glycogen and
10% from plasma glucose), and proteins (10%) [PMID: 12070189].
440
Another study reported
carbohydrate (rather than fat) oxidation represented the major fuel for thermogenesis in the cold
(51%) [PMID: 2767069].
441
Lipolysis and free fatty acid turnover are greatly increased by cold
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
53
stress, but only about half the rate of free fatty acid turnover is ultimately oxidized [PMID:
9895020].
442
Certain metabolic conditions (obesity and diabetes in women) are associated with an
abnormal metabolic response to cold stress, possibly related to abnormal thyroid responses
[PMID: 3254262].
443
A study of obese women exercising in cool water concluded that while
cold exposure does not increase caloric expenditure significantly in obese individuals, exercising
regularly in cool water may motivate obese people to exercise at higher intensity for thermal
comfort [PMID: 7068314].
444
C7.4.2.4.2. Appetite
Decrease in appetite and food intake has been noted in cold exposure at high altitudes
[
PMID: 1582718];
445
however, this appears to be due to hypobaric hypoxia [PMID:
10409600].
446
Conversely, although a cold-induced increase in appetite may be expected,
evidence for such a phenomenon is poor [PMID: 10817145].
447
Water availability may affect
food intake, as noted previously (see
above).
C7.4.3. Cardiovascular
C7.4.3.1. Shunting
Cold constricts cutaneous blood vessels by increasing the reactivity of smooth muscle
alpha (2)-adrenergic receptors [PMID: 10749700].
448
Vasoconstriction via the sympathetic
nervous system is most pronounced in the extremities, but is minimal in the head and neck
[PMID: 1811574]
449
[PMID: 2221434].
450
C7.4.3.2. Blood Pressure
Cold exposure increases blood pressure [PMID: 11374119].
451
Exposure to cold air
increased average systolic and diastolic pressures approximately 20 millimeters of mercury each
[PMID: 11214769].
452
Blood pressure is noted to be higher in winter than in summer [PMID:
9314429].
453
C7.4.3.3. Heart Rate and Cardiac Output
Heart rate may be lower or unchanged during exercise in the cold [
PMID: 1925184].
454
For those with coronary artery disease, heart rate during exercise in the cold may be unchanged
or higher [PMID: 8529083].
455
Cardiac output increases with cold exposure (e.g., 10% increase
at 50° F or 10° C) [PMID: 3968010].
456
Cold-water immersion including the face triggers the
diving reflex (bradycardia response) [PMID: 11816961].
457
Immersion of only a hand causes
increased heart rate [
PMID: 11209666].
458
Cold increases the risk of arrhythmia during exercise
[PMID: 11505864].
459
C7.4.3.4. Oxygen Consumption
Exercise oxygen consumption is generally higher in the cold, but the difference between
warm and cold environments becomes less as workload increases [PMID: 1925184].
460
Plasma
volume decreases on exposure to cold stress [
PMID: 3629738].
461
C7.4.4. Respiratory Tract and Ventilation Changes
Acute or chronic cold exposure can cause bronchoconstriction, airway congestion,
secretions, and decreased mucociliary clearance (actively in cold-induced or exercise-induced
asthma), resulting in decreased baseline ventilation and respiratory chemosensitivity. Cold
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
54
exposure increases pulmonary vascular resistance. Chronic cold exposure results in increased
numbers of goblet cells and mucous glands, hypertrophy of airway muscle tissue, and increased
muscle layers of terminal arteries and arterioles. [PMID: 7487830].
462
Minute ventilation is substantially increased upon initial exposure to cold [
PMID:
1925184].
463
Acute cold stress exposure early in acclimatization causes a decrease in ventilation
parameters.
3
As acclimatization continues, there is a gradual recovery continuing up to 9 weeks
[PMID: 8468097].
464
C7.4.5. Shivering
Shivering is the body’s reserve mechanism for dealing with extreme heat loss, as
sweating is the body’s mechanism for removing heat in excessive heat stress conditions.
C7.4.5.1. Metabolism of Shivering
Shivering can increase the metabolic rate to a maximum of approximately five times the
resting rate [PMID: 11394237].
465
Shivering can generate heat at a rate of 10 to 15 kilojoules per
minute, but it impairs skilled performance, while the resultant glycogen usage hastens the onset
of fatigue and mental confusion [PMID: 3883460].
466
Thermoregulatory responses of cold stress
exposure are not related to muscle glycogen levels of major skeletal muscle groups; other
metabolic substrates may enable sparing of muscle glycogen during shivering [PMID:
2732173].
467
Hypoglycemia may delay shivering onset until core temperature is lower than what
would cause shivering with normal blood sugar levels [PMID: 8964720].
468
C7.4.5.2. Peak Shivering Metabolic Rate Equation
An equation to calculate the peak shivering metabolic rate has been formulated as follows
[PMID: 11394237].
469
Peak shivering metabolic rate (in milliliters of oxygen per kilogram per minute) =
30.5 + 0.348 x maximal oxygen uptake (in milliliters of oxygen per kilogram per minute) –
0.909 x body mass index (in kilograms per square meter) –
0.233 x age (in years).
C7.4.6. Fatigue
Vasoconstrictor responses to cold, but not shivering responses, are impaired after
multiple days of severe physical exertion [PMID: 11181604].
470
Fatigue induced by chronic
overexertion sustained over many weeks delays the onset of shivering until body temperature is
lower than in rested individuals [PMID: 11282320].
471
These findings suggest that susceptibility
to hypothermia is increased by exertional fatigue [
PMID: 11181604].
472
C7.4.7. Circadian Rhythm (Body Clock)
Cold exposure at night lowers core body temperature and increases blood pressure more
than cold exposure in the afternoon; skin temperatures, however, decrease less after cold
exposure at night than they do after cold exposure in the afternoon, and may explain the
difference in core temperatures [
PMID: 11374119].
473
Researchers report sensations of thermal
cold and pain and manual dexterity are less after cold exposure at night than during the day,
3
Vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in the first second (FEV
1
), peak
expiratory flow rate (PEFR), and maximum voluntary ventilation (MVV).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
55
which were felt to suggest that there is an increased risk of both hypothermia and accidents for
those who work at night [PMID: 11374119].
474
C7.5. Acclimatization
C7.5.1. Acclimatization and Acclimation
Acclimatization refers to the adaptation to cold or heat stress that occurs after repeated
exposure to cold or heat stress conditions. Acclimation refers to adaptation that occurs after
laboratory-controlled exposure to cold or heat stress.
4
C7.5.2. Effects of Acclimatization
The following effects of cold acclimatization (or acclimation) have been observed.
An increase in the delay for the onset of shivering (approximately twice as long before
shivering starts) [PMID: 3597234];
475
A slight (less than 0.5° F) decrease of core body temperature levels at the onset of
shivering [PMID: 3597234];
476
Lower core body temperature in thermoneutrality (less than half a degree F) [PMID:
3597234];
477
A decrease of heat debt calculated from the difference between heat gains and heat
losses (by about one third) [PMID: 3597234];
478
Reduced sensitivity to the pressor effect of norepinephrine [PMID: 8299617];
479
Reduced cold-induced muscle tenseness [PMID: 8299616];
480
Less shivering on cold exposure [PMID: 1483764];
481
Lower central and peripheral body temperatures at rest and during cold immersion
[PMID: 8765994];
482
Delayed metabolic response to cold [PMID: 8765994];
483
Attenuated subjective shivering [PMID: 8765994];
484
Lowered cold sensation [PMID: 8765994];
485
Increased vasoconstriction, evidenced by lowered skin temperature [PMID:
8765994];
486
Increased plasma potassium concentration during cold exposure (no change in plasma
sodium concentration) [
PMID: 3629738];
487
Increased rate of rewarming [PMID: 655993];
488
Lowered diastolic pressure and an increase in peripheral vasoconstriction [PMID:
8891513];
489
Altered control of blood pressure during acute cold stress (in one study of repeated
cold-water exposures, blood pressure increased significantly during the first cold-
water exposure, but not during the last cold-water immersion) [
PMID: 3388627];
490
Increased minute ventilation during cold air and cold-water exposure [PMID:
3388627];
491
Lower oxygen consumption in cold air (but not in cold water) [PMID: 3388627];
492
Cold acclimation attenuates the onset of metabolic heat production during cold air
exposure [PMID: 3388627].
493
4
While “acclimatization” and “acclimation” are not identical, use in this text will be generally as used by authors.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
56
C7.5.3. Limitations of Acclimatization
Overall, the effects of cold acclimatization (on tolerating cold exposure) are minimal
compared to the effects and advantages of heat acclimatization (on tolerating heat exposure).
Maximal aerobic and anaerobic performances are not altered by acclimatization
[PMID: 8765994].
494
Cold acclimation does not affect the minute ventilation - carbon dioxide production
relationship or the pattern of breathing in cold air or water [PMID: 3388627].
495
Cold acclimation does not alter the magnitude of metabolic heat production [PMID:
3388627].
496
Cold acclimation has no effect on cardiac output or arterial-venous oxygen difference
[
PMID: 3388627].
497
Cold acclimation, when developed by cold-water immersion, does not influence
vascular fluid responses to cold stress (increased urinary excretion rate of both sodium
and potassium during cold exposure) [
PMID: 3629738].
498
Acclimatization does not induce non-shivering thermogenesis in adults [
PMID:
8299617].
499
C7.5.4. Development of Acclimatization
Repeated cold-water immersion can induce the development of an insulative type of cold
acclimation in man, specifically including changes in thermoregulation [PMID: 3710973].
500
However, vascular fluid responses to cold stress are not altered by repeated cold-water
immersion [PMID: 3629738].
501
C7.5.4.1. Altitude
Thermoregulation efficiency of man deteriorates at high altitude; general cold exposure
acclimatization at high altitude may take much longer in those not native to high altitudes, or
may even be unattainable [PMID: 655993].
502
C7.5.4.2. Local (Rather than Whole Body) Acclimatization
Exposure to severe local cold leads to adaptive responses in which discomfort and
autonomic activity are reduced [PMID: 3057321].
503
Local cold acclimation induces a local cold
adaptation (decreased reduction in skin temperature during cold exposure) by significantly
decreased plasma concentrations of norepinephrine [
PMID: 8781852].
504
Local cold
acclimatization is possible regardless of what climate a person (or a person’s ancestors) is from
[
PMID: 1297856].
505
C7.5.5. Habituation
Exposure to systemic moderate cold causes a reduction in heat production, in shivering,
and in discomfort through a process known as habituation [
PMID: 3057321].
506
Habituation is
“the method by which the nervous system reduces or inhibits responsiveness during repeated
stimulation” [Stedman’s].
507
Habituation to cold stress results from repeated brief exposures to
cold. Rather than a series of physiologic changes, it is an enhanced tolerance to the cold due to
decreased sympathetic activity, which is thought to be a diminished alarm reaction [
PMID:
1483764
].
508
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
57
C7.5.6. Non-Shivering Thermogenesis
In newborn humans and in many mammals, brown adipose tissue is metabolized to
maintain body temperature (non-shivering thermogenesis) [PMID: 1891665].
509
However,
during metabolic cold acclimation, brown adipose tissue is not a major site for non-shivering
thermogenesis in adult humans [PMID: 7744360].
510
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
58
Chapter 8:
C8. Prevention of Cold Stress Injuries
C8.1. Measurement of Cold Stress Effects on the Body
C8.1.1. Core Body Temperature
The most reliable method generally available in hospital settings for determining core
body temperature is the esophageal thermometer (see section on
Prevention Of Heat Stress
Injuries). In field settings, rectal temperatures provide a reasonable approximation of core body
temperature. Tympanic and oral temperature readings have been subject to variation due to
exposure to air and/or water.
Esophageal temperatures, but not rectal or tympanic temperatures, have been found to be
representative of cardiac temperature [PMID: 6322264].
511
C8.1.2. Skin or Local Temperature
The need for accuracy is less in determining the temperature of the extremities exposed to
cold stress. (In other words, knowing whether a toe is 25° F or 15° F, -3.9° C to -9.4° C, is not as
critical to patient management as knowing whether core body temperature is 95.4° F or 89.4° F,
35.2° C to 31.9° C, although the absolute temperature difference of the former is much greater.)
Even a gross approximation, such as whether an extremity “feels frozen,” may be adequate to
guide appropriate treatment. Accurate documentation of skin temperature, however, requires the
use of a thermometer.
C8.1.3. Cold Strain Index
A cold strain index based on rectal and mean skin temperatures has been proposed
[PMID: 10444564],
512
but has been shown to require further refinement before being considered
valid for widespread use in quantifying cold strain [PMID: 11705759].
513
C8.2. Identifying Risk Factors
Prevention of cold stress injuries begins with recognition of risk factors. Arctic locations
or freezing weather are not the only conditions in which cold stress injuries occur. Severe
hypothermia in a tropical setting has been reported [
PMID: 9791596].
514
C8.2.1. Protective Clothing
Collectively, the limited experimental work and the results of simulation modeling argue
against any increased risk of hypothermia associated with wearing nuclear, biological, or
chemical (NBC) protective clothing while working in the cold. However, wearing NBC
protective clothing during strenuous activity in cold weather may increase the risk of
hyperthermia, and cause sweat accumulation in clothing which may compromise insulation and
increase the risk of hypothermia during subsequent periods of inactivity [
PMID: 10685594].
515
C8.2.2. Ointments, Lotions, Creams, Emollients, etc.
Application of ointments to the face has been shown not to offer protection against
frostbite of the head in cold climates [PMID: 10086864].
516
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
59
C8.2.3. Vasospastic Syndrome
People with vasospastic syndrome have cold hands and feet and abnormal
vasoconstriction after local cold exposure [PMID: 11463418].
517
C8.2.4. Motion Sickness
Motion sickness attenuates the vasoconstrictor response to skin and core cooling, thereby
enhancing heat loss and the magnitude of the fall in deep body temperature; motion sickness may
predispose individuals to hypothermia, and have significant implications for survival time in
maritime accidents [
PMID: 11533150].
518
C8.2.5. Shapiro’s Syndrome
Shapiro’s Syndrome (Spontaneous Periodic Hypothermia) is a very rare disorder of
temperature regulation, rather than merely a risk factor for hypothermia (see previous section on
Central Nervous System (CNS) Abnormalities).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
60
Chapter 9:
C9. Diagnosis and Treatment of Cold Stress Injuries
C9.1. Dermatological (Skin) injuries
C9.1.1. Conditions Unmasked or Exacerbated by Cold Exposure
C9.1.1.1. Acrocyanosis
Acrocyanosis (also known as Crocq's disease), “a circulatory disorder in which the hands,
and less commonly the feet, are persistently cold and blue” [Stedman’s],
519
is more intense in
cold weather. Symptoms are permanent and painless cyanosis of extremities, local hypothermia,
permanent sweatiness, and elastic infiltration of the integument; capillaroscopy visualizes
capillarovenular stasis [PMID: 9814068].
520
Some forms of acrocyanosis are related to
Raynaud's phenomenon (see below).
C9.1.1.2. Rosacea
Rosacea (also known as acne erythematosa and acne rosacea) is a condition of the nose
and cheeks involving dilation of blood vessels and follicles. Rosacea may be exacerbated by cold
weather [PMID: 12182520].
521
C9.1.1.3. Cold Agglutinin Disease
Cold agglutinin disease is a symptom-producing monoclonal B-cell lymphoproliferative
disorder [PMID: 9201236,
522
PMID: 11722415].
523
The dysfunction of auto-reactive B-cell
clones may be triggered by infection of some viruses and bacteria, or by certain medications
[PMID: 8890588].
524
Cold agglutination may also be associated with underlying disease
(lymphoma, post-mycoplasma or infectious mononucleosis infections) [Schrier].
525
Cold agglutinin disease may present as an autoimmune hemolytic anemia, characterized
by high titers of serum IgM agglutinins (antibodies) maximally active at 39.2° F (4° C)
[Schrier].
526
It may be difficult to draw blood, and the red cells may visibly agglutinate in a cold
syringe and on the blood smear. Symptoms are livedo reticularis of the thighs and a history of
acrocyanosis and Raynaud's phenomenon upon cold exposure [PMID: 11455160].
527
(See Cold
Agglutinin Disease
, below, for a further discussion.)
C9.1.1.4. Cold Panniculitis
Cold panniculitis is a skin condition with red, cold, indurated plaques or nodules which
appear one to three days after exposure to low temperatures and resolve spontaneously within
several weeks without scarring [
PMID: 9830269].
528
Also known as Haxthausen's disease in
children [
PMID: 3370518],
529
cold panniculitis can be caused by exposure of the skin to cold,
including cold packs. It is the consequence of lipid crystallization within adipocytes [PMID:
10667045].
530
C9.1.1.5. Xerosis
Impaired desquamation may be one consequence of cold exposure, resulting in xerosis
(dry skin); xerosis on the limbs due to impaired desquamation is not rare [PMID: 10667045].
531
C9.1.1.6. Cold-induced Urticaria
Cold-induced urticaria (hives) is a form of physical urticaria that develops on cold
exposure in susceptible individuals. Most cases are of unknown etiology (primary or idiopathic),
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
61
and management includes avoidance measures and antihistamines. Life-threatening symptoms
necessitate carrying a self-administered injectable epinephrine [PMID: 11409259].
532
C9.1.2. Chilblain
Chilblain (chilblains, Milker’s chilblains, erythema pernio, perniosis) is a vascular
(erythrocyanotic) discoloration of the acral skin occurring after exposure to the cold (generally
moist cold). It is most common in young women although it can happen at every age, and
relapses characteristically in autumn and winter [PMID: 9814070].
533
Chilblain results from
reversible alterations of the dermal vasculature [PMID: 10667045],
534
including an obstructive
and thrombotic microangiopathy, especially of venules [
PMID: 3958629].
535
Histology shows
vascular and perivascular capillary and venular lymphocyte infiltrates without necrosis [
PMID:
1431611].
536
It also may be associated with underlying connective tissue disorders (specifically
lupus erythematosus [PMID: 11388094]),
537
especially if it lasts longer than one month [PMID:
11388094].
538
Symptoms include pruritic, painful (especially burning) red patches on the fingers and/or
toes, generally bilaterally. Sunlight may aggravate the lesions [PMID: 8474715].
539
Ultraviolet
irradiation can induce cutaneous lesions during winter [PMID: 10667045].
540
Laboratory studies
are normal. Diagnosis may be difficult [PMID: 8474715].
541
The differential diagnosis includes
lupus, cold urticaria, acrocyanosis, erythromelalgia (erythermalgia, Gerhardt's disease; Mitchell's
disease; red neuralgia; rodonalgia), vasculitis and the Blue Toe Syndrome (tissue ischemia
secondary to cholesterol crystal or atherothrombotic embolization leading to the occlusion of
small vessels [PMID: 12555011])
542
[PMID: 1431611].
543
Spontaneous healing is common when
spring arrives and relapse is frequent during the following winters [PMID: 1431611].
544
Significant scarring may result [PMID: 8474715].
545
Treatment is removal from the cold (including passive warming). Nifedipine may hasten
resolution of symptoms, signs, and biopsy findings [PMID: 2647123].
546
Prevention includes
prophylactic measures against cold; nifedipine is also suggested as a prophylactic (vasodilator)
therapy [PMID: 8474715].
547
In more severe cases, thyrocalcitonin and hemodilution might be
helpful [PMID: 1431611].
548
C9.2. Injuries of the Extremities Due to Cold Exposure
C9.2.1. Frostbite
Frostbite (congelation, dermatitis congelationis, “Teruel feet” [PMID: 16155617])
549
is a
localized cold injury, generally of exposed or inadequately protected acral areas, resulting in
tissue destruction due to freezing or sub-freezing temperatures. Victims complain of numbness,
coldness, pain, or loss of use of the affected area, and are risk for other cold-related injuries, such
as hypothermia and snow blindness.
C9.2.1.1. Mechanisms (Pathophysiology) of Frostbite
The central pathogenic mechanism is ice crystal formation in tissue, resulting in cellular
injury; ensuing and concomitant ischemic anoxia and acidosis contribute to the injury (see
Figure
7
). As rewarming (thawing) of frozen tissue allows re-perfusion, vascular permeability and
intravascular thrombi formation result in further anoxic damage. When rewarming is done
gradually, marginal tissue ice crystal formation may recur, resulting in further damage. Similarly,
freeze-thaw-refreeze (for example, when a frostbite victim is warmed, but then is exposed to
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
62
further freezing) injuries may be worse than cases left frozen until thawing can be done without
re-exposure to freezing cold.
C9.2.1.1.1. Hunting reaction
The hunting reaction (also called the Lewis hunting reaction, the hunting phenomenon,
and the hunting response) occurs when extremities are cooled (for example, immersed in water at
41° F to 59° F, or 5° C to 15° C). Vasoconstriction is alternated with vasodilation in irregular
repeated sequences in digital blood vessels exposed to cold [Stedman’s].
550
The mechanism may
be a cold-induced increased affinity of the post-junctional alpha-adrenoceptors for
norepinephrine, leading to vasoconstriction; vasoconstriction leads to further decreased tissue
temperature and sympathetic nerve conduction, leading to vasodilatation; vasodilation restores
blood flow, nerve conduction is reestablished, and increased affinity of the alpha-adrenoceptors
for norepinephrine leads to renewed vasoconstriction [PMID: 6131011].
551
When core
temperature is threatened, the hunting response is superseded by vasoconstriction alone
[Gonzalez].
552
Figure 7 - Pathophysiology of Frostbite
C
old Exposure
Tissue
Freeze
Vasoconstriction
Blood
Hyperviscosity
Blood Shunting
Ice Crystal
Formation
Cellular
Injury
Localized
Metabolic
Acidosis
Tissue Anoxia
Microthrombi Hypercoag-
ulability
Aggregation of Platelets
and Red Blood Cells
Edema
Increased
Capillary
Permeability
Frostbite
Injury
Recover
y
Necrosis
Reduced
Blood Flow
Blood
Stasis
Pathophysiology o
f
Frostbite
Adapted from Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261
cases). Int J Sports Med 1992 Oct;13 Suppl 1:S193-6. Used with permission.
C9.2.1.2. Frostbite Risk Factors
Low air temperatures and high wind speeds are associated with an increased risk of
freezing of the exposed skin; as the skin surface temperature falls from 23.4° F (-4.8° C) to 18° F
(-7.8° C), the risk of frostbite increases from 5% to 95% [
PMID: 9018520].
553
A review of cold-
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
63
weather injuries among soldiers noted the following frostbite risk factors: Negro race, inadequate
clothing, wet clothing, dehydration, inactivity, fatigue, and previous cold weather injury [PMID:
9433082].
554
Specific factors associated with increased risk of frostbite include not wearing a hat
with earflaps, not wearing a scarf, using protective ointments, having hands and feet that sweat
profusely, and being transported in the open or in open vehicles under windy conditions [PMID:
8541749].
555
The Marine ski-march leather boot and smoking were related to foot cold injuries
in a winter mountain training exercise [PMID: 11149059].
556
Smoking has been shown to be a
contributing factor in high altitude frostbite, as has peripheral vascular disease and altitude (with
greatest risk above 17,000 feet above sea level) [
PMID: 9623370].
557
A review of peacetime
military frostbite injuries showed no risk associated with gender or rank [
PMID: 1361671].
558
In civilian populations in the United States, homelessness, alcohol use, psychiatric
illness, and motor vehicle breakdown have been associated with frostbite [PMID: 9456445].
559
Workers with vibration white finger have been found to be at increased risk of frostbite [PMID:
8318122].
560
C9.2.1.3. Classification of Frostbite
Traditional classification of frostbite injuries (first, second, third, and fourth degree) is
similar to (but not the same as) classification of burns. A recent classification based on early
bone scan results and lesion characteristics has been proposed, but has not been widely accepted
[PMID: 11769921].
561
In an investigation of contact cooling of the hand, researchers observed what may have
been frostnip or even early frostbite, with severity depending on the finger involved and direct
contact with a cold object. Immediately after hand exposure to cold metal objects (-20° F or –
28.9° C), finger skin showed white patches that rapidly disappeared on rewarming. Some areas
had a burning sensation, associated with diffuse redness with a slightly cyanotic hue. After 24
hours, scattered patches of redness and hardening of skin in contact areas were noted. The little
finger tip pad was mottled gray with a pinkish cast surrounded by erythema, painful to slight
pressure and not anesthetic, although light touch was diminished. Pink areas of skin blanched
with pressure and rapidly recovered pinkness. Peeling skin developed in many areas of metal
contact, while blistering developed over the ball of the little finger [Daniels].
562
C9.2.1.3.1. Frostnip
This is the mildest freezing injury of the skin, and involves freezing of water on the skin
surface. The skin is reddened and may be swollen. Recovery is complete (similar to a mild
sunburn) with removal from cold exposure.
C9.2.1.3.2. First Degree Frostbite
First degree frostbite is a partial thickness injury of the skin, sparing deeper structures. It
is characterized by erythema, edema, and hyperemia. There is no blister formation or necrosis.
Victims complain of pain (for example, a burning sensation).
Prior to thawing, in frostbite that is severe first degree or worse, skin is gray or whitish
(often described as “waxy” or “waxy-white”).
Swelling occurs within 3 hours of rewarming and may last 10 days. Desquamation starts
in about a week, and may last up to one month. Resolution is expected to be complete and
without scarring.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
64
C9.2.1.3.3. Second Degree Frostbite
Second degree frostbite is characterized by blisters or blebs, which may not form until
after rewarming, and by erythema and edema [PMID: 10998830].
563
It is a full-thickness injury
that spares subcutaneous tissue. Blisters (which usually form after rewarming) contain serous
fluid. Victims may complain of numbness.
There is no permanent tissue loss. Sequelae include increased cold sensitivity,
hyperhidrosis (“sweaty” feet or hands), paresthesias, pain, and necrosis of pressure points on the
feet.
The vast majority of frostbite injuries in the military are either first or second degree,
according to a recent review of Army Experience in Alaska [PMID: 9433082].
564
C9.2.1.3.4. Third Degree Frostbite
Third degree frostbite includes injury to the skin and subcutaneous tissue. Hemorrhagic
blisters may be present (usually after rewarming), with bluish skin and skin necrosis. Initially,
involved areas are anesthetic, becoming painful on rewarming.
Skin loss by sloughing is expected, with permanent tissue loss and scarring.
C9.2.1.3.5. Fourth Degree Frostbite
Fourth degree frostbite involves skin, subcutaneous tissue, and deeper structures,
including bone, tendon, or muscle. Affected areas are anesthetic, even after rewarming, although
severe paresthesias may develop days to weeks later [NAVEDTRA 13147-A].
565
C9.2.1.4. Evaluation
Physical examination should document core body temperature, temperature of the
involved area (if an exact temperature cannot be taken, then subjective descriptors such as
“frozen,” “cold,” “cool,” etc., may be used), presence of blisters and color of blister fluid, and
“feel” of the affected area (e.g., waxy, hard, etc.). Peripheral pulse and capillary refilling should
be documented and checked repeatedly as the injured area is rewarmed. Neurological exam
(including two-point discrimination, vibration, and movement) also should be checked and
followed.
The appearance of superficial tissue is often an unreliable indicator of deep-tissue
viability in cases of frostbite [
PMID: 11822694].
566
Experienced clinicians state that 4 to 5 days
may be required to ascertain whether lesions involve superficial or deep freezing; if there has
been tissue necrosis, approximately one to two months may be required to define the limits of
necrosis [
PMID: 1483773].
567
Technetium (Tc)-99 bone scanning (bone scintigraphy) has become the standard imaging
study employed within the first several days to assess tissue perfusion and viability [
PMID:
9088467].
568
Two-phase technetium-99m hydroxymethylene diphosphonate bone scans have
been used in evaluation of frostbite and treatment follow-up. Correlation between absence of
tracer uptake in the phalanges and later amputation was shown to have high sensitivity (0.99) and
high specificity (0.96) in one study of severe frostbite [
PMID: 10853803],
569
but not in a study of
mild to moderately severe frostbite using technetium-99m pertechnetate [
PMID: 11926378].
570
Successful use of technetium-99m-sestamibi scintigraphy in evaluation of frostbite has also been
reported [PMID: 11822694].
571
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
65
Magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) were
felt superior to Tc-99 bone scans in a small study (two cases) of severe frostbite injury. The
authors felt MRI and MRA offered the advantages of allowing direct visualization of occluded
vessels, imaging of surrounding tissues, and of showing a more clear-cut line of demarcation of
ischemic tissue [PMID: 9088467].
572
C9.2.1.5. Treatment of Frostbite
C9.2.1.5.1. Rewarming
Initial treatment is immediate removal from cold exposure. If that cannot be done, further
treatment (rewarming) should be delayed to avoid freeze-thaw-refreeze-thaw, which may result
in worse injury than a single freeze-thaw. Rewarming of frostbitten lower extremities should not
be done if the person must walk to get to medical treatment. Rewarming should never be done
using an open flame [CHIPPM TN/02-2].
573
Rapid rewarming in water (as opposed to gradual rewarming) is the definitive treatment
for frostbite [PMID: 10791170].
574
Water temperatures from 96.8° F (36° C) [PMID:
1483773]
575
to 108° F (42.2° C) [PMID: 9460447]
576
have been recommended. Some clinicians
add a mild antiseptic to the water, and limit immersion to 20 to 30 minutes twice daily [PMID:
1483773].
577
Rewarming may be quite painful and require analgesics and sedatives [PMID:
9556318].
578
Once thawing is complete, the injured part must be kept clean and dry and protected from
further trauma. All patients with cold injuries of the lower extremity are litter patients. In the
field, patients with more than first degree frostbite should be evacuated as soon as possible to a
definitive treatment facility, since the extent of injury may not be readily apparent and
convalescence is usually prolonged.
C9.2.1.5.2. Rest
Rest of the affected limb or limbs should be enforced until recovery. If lower limbs are
involved, bed rest is required.
C9.2.1.5.3. Blood Flow
“Hemodilution” (actually, optimizing hydration and circulating volume) is done to
address dehydration (often present, especially in high altitude-related cold exposure injuries) and
microcirculation defects [
PMID: 1483773].
579
Dextran is often used to limit edema [PMID:
1483773].
580
Thrombolytics have been used in treatment of frostbite [
PMID: 8214384].
581
A report
notes a smaller area of damaged tissue using fibrinolysin in combination with other drugs in a
clinical setting [
PMID: 2165688].
582
Limited animal data indicates streptokinase administered
within 48 hours of frostbite results in less tissue damage from frostbite [PMID: 2820216].
583
Anticoagulants have been advocated in the treatment of frostbite [PMID: 8214384]
584
[
PMID: 1483773].
585
Heparin has been used, with benefits possibly related to anti-inflammatory
effects rather than from anticoagulation [PMID: 1483773].
586
A recent series reported positive
results using heparin and IV tissue plasminogen activator in treatment of severe frostbite [
PMID:
16394908].
587
Other anti-inflammatory agents (non-steroidals such as ibuprofen and aspirin) have also
been recommended to decrease systemic levels of thromboxane [PMID: 2243830]
588
(suspected
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
66
to have a role in frostbite tissue damage [PMID: 7204918]).
589
Several other agents targeting
thromboxane and prostaglandin (to inhibit the “arachidonic acid cascade” [PMID: 3631670])
590
have been promoted, including Aloe vera [PMID: 2243830],
591
methimazole [PMID:
3631670],
592
and methylprednisolone [PMID: 3631670].
593
Some authors recommend early
aspiration of blister fluid [
PMID: 9734425],
594
on the grounds that the thromboxane and
prostaglandin known to play a role in burn pathogenesis have been found in frostbite blisters
[PMID: 7204918].
595
However, it has not been established that the presence of those substances
in frostbite blisters worsen recovery outcome, or that early blister aspiration improves outcome.
Pentoxifylline to increase red blood cell flexibility also has been suggested for use in
frostbite [PMID: 11070801].
596
Vasodilators (buflomedil hydrochloride, naphtidrofuryl, or ketanserin) have been
advocated by some authors, but efficacy in frostbite is not established [PMID: 1483773].
597
Similarly, although nifedipine has been useful in treating (and suggested for prophylaxis against
[
PMID: 8474715])
598
Chilblain [PMID: 2647123],
599
its efficacy in frostbite is not established in
the scientific literature.
Smoking is absolutely prohibited during recovery from frostbite [NAVEDTRA
13147-A].
600
C9.2.1.5.4. Neurological
Sympathetic blockade may be used to both decrease sympathetic tone and relieve pain
(e.g., epidural bupivacaine [PMID: 1483773]),
601
or for pain relief alone (e.g., continuous
epidural morphine [PMID: 9556318])
602
[PMID: 3659437]
603
[PMID: 10459266].
604
However,
effectiveness in improving outcome is not established [PMID: 7411663].
605
C9.2.1.5.5. Hyperbaric Oxygen
Hyperbaric oxygen has been successfully used on frostbite [PMID: 11348755].
606
C9.2.1.5.6. Surgery
Debridement without anesthesia may be done to help visualization of tissue [PMID:
1483773].
607
Surgical amputation, if necessary, should be delayed 60 to 90 days (minimum of 3
weeks), unless sepsis occurs [
PMID: 1483773]
608
[NAVEDTRA 13147-A].
609
C9.2.1.5.7. Prevention of Infection
Tetanus toxoid booster is appropriate, if required, as tetanus is a known complication of
frostbite [
PMID: 8323232].
610
Prophylactic antibiotics have not been found to prevent wound
infection [PMID: 8356126].
611
Meticulous attention should be given to signs of infection. Mild antiseptics may be added
to whirlpool baths. Blisters that may form do not require removal unless they impede joint
motion, are large [
PMID: 6884849],
612
or show signs of infection.
C9.2.1.5.8. Recovery
Those who apparently have recovered from frostbite often have sequelae, including
hypersensitivity to cold, numbness, declined sensitivity of touch, and decreased working ability
with affected fingers. In one study, the skin temperature of frostbitten areas exposed to cold air
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
67
decreased more quickly and reached lower values than in healthy control subjects [PMID:
10998831].
613
Pre-thaw
Prevent pressure on the injured part as much as possible
Do not rub or massage
Stay off feet if possible (if patient cannot be carried, walking is better than hypothermia)
Do not try to move joints in areas already frostbitten
Remove victim from cold exposure ASAP
Do NOT thaw or warm until there is NO chance of re-freezing
Maintain adequate hydration
Thawing
Immerse in warm water (96.8° F to 108° F)
Tetanus booster if needed
Ibuprofen 400 mg by mouth every 4 hours
Establish IV access, and maintain adequate hydration (orally or IV)
Parenteral analgesics as needed
Heparin IV
Encourage gentle motion of the affected part, but do not massage or force flexion or extension
Consider: pentoxifylline, fibrinolysin, streptokinase, hyperbaric oxygen, dextran
Smoking is prohibited
Post-thaw
Elevate injured part and keep dry
Leave vesicles (blisters) intact unless signs of infection
Debride broken vesicles and apply topical antibiotic
Limited debridement without anaesthesia (and that does not cause victim pain!) as necessary to
visualize tissue
Surgery after 2 or 3 months if necessary
Smoking is prohibited until no further recovery is expected, and then is strongly discouraged
Table 11 - Frostbite Rewarming Protocol
C9.2.2. Trench Foot (Trenchfoot)
The Textbook of Military Medicine describes four immersion foot syndromes: trench
foot, immersion foot, tropical immersion foot, and warm water immersion foot. Trench foot is
distinguished from immersion foot only by whether or not the foot was actually immersed, and
not just wet.
614
(The term “immersion foot” as used here is to be distinguished from the term
“immersion foot” used to refer to “tropical immersion foot” and “warm weather immersion
foot,” both water-related foot injuries not related to cold exposure, that have also been called
such colorful names as “swamp foot,” “jungle rot,” etc. [
PMID: 2012466].)
615
Trench foot (immersion foot) is a cold injury to extremities exposed to non-freezing
temperatures, usually prolonged exposure involving moisture. On exposure to water from 32° F
to 59° F (0° C to 15° C), clinical trench foot will develop if exposure lasts 12 to 48 hours
(depending on the water temperature). Contributing factors include nutritional deficiency, trauma
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
68
(rubbing or walking on affected feet), wind, improper clothing type and integrity, circulatory
stagnation and tissue anoxia from dependency, inactivity, hemorrhage, shock, and improper
technique used to rewarm an injured limb.
616
In addition to military personnel, those involved in
adventure tourism and the homeless are at particular risk for trench foot [
PMID: 12363167].
617
Trench foot is a very serious injury that may result in permanent nerve or tissue damage,
or, untreated, may require amputation [
PMID: 6115374,
618
CHIPPM TN/02-2].
619
In contrast to
frostbite, trench foot injuries that have been rewarmed intermittently during cold exposure may
be less severe,
620
(hence the need to distinguish between non-freezing and freezing cold exposure
injuries).
C9.2.2.1.1. Stages of Trench Foot
Trench foot has three clinical “stages”: prehyperemic, hyperemic, and posthyperemic
[MilDerm].
621
Symptoms begin with cold, then numbness, paresthesias, and itching. Weight
bearing may be painful. With continued cold exposure, numbness progresses to anesthesia, with
the classic complaint of “walking on blocks of wood.” Signs include pallor, mottling or purple
coloration, swelling, vesicles, bullae, and edema. There may be a "water-line" coinciding with
the water level in the boot [CHIPPM TN/02-2].
622
This is the “prehyperemic stage.”
On or after rewarming, sensation returns proximally first, with paresthesias and burning
or throbbing pain. Heat sensitivity is increased. Hypoesthesia, further swelling, and erythema
may develop. Mottling and discoloration may appear or increase. This is the hyperemic or
inflammatory stage. Blisters, circulatory compromise, local hemorrhage, and ecchymosis may
characterize severe cases. Recovery of less severe cases may take up to 4 weeks, with exfoliation
and possible scarring [MilDerm].
623
More serious cases have a “posthyperemic stage,” a prolonged post-inflammatory phase
involving compromised blood supply. Signs and symptoms include cyanosis, mottling, pain
(distal and small joints), hyperesthesia, paresthesia, anesthesia, atrophy of skin and muscles,
osteoporosis, and contractures (especially clawfoot). Vascular and microvascular abnormalities
related to sympathetic vasoconstriction, thrombosis, and increased vascular permeability may be
involved [MilDerm].
624
Trench foot may result in a peripheral neuropathy, and the proposed mechanisms of
injury include direct axonal damage, ischemia, and ischemia-reperfusion. In mild or early cases,
large myelinated fibers are preferentially damaged, while small myelinated and unmyelinated
fibers are relatively spared. Nerve damage starts proximally and extends distally with time
[
PMID: 8712655].
625
In severe non-freezing cold injury cases, all nerve populations (myelinated
and unmyelinated) may be damaged [PMID: 9306996].
626
Axonal degeneration has been
attributed to free radicals released during cycles of ischemia and reperfusion; however, the
administration of commonly used antioxidants has not been found to prevent cold nerve injury
[
PMID: 12363167].
627
C9.2.2.1.2. Treatment of Trench Foot
Treatment consists of bed rest, elevation of the legs, and air-drying at room temperature,
while keeping the rest of the body warm (i.e., treating or preventing hypothermia). Rewarming of
trench foot should be more gradual, passive, and at temperatures lower than recommended for
frostbite. Careful foot hygiene is important. Antibiotics may be used for signs of infection
(covering for Staphylococcus, Streptococcus, and Pseudomonas until culture results are available
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
69
[PMID: 2012466]).
628
Non-steroidal or even narcotic analgesics may be necessary. Tetanus
immunization should given if not up to date.
Other forms of therapy suggested for frostbite (rapid rewarming, low molecular weight
dextran, sympathetic blockade, continuous epidural anesthesia, anticoagulation, and regional
sympathectomy) have not been specifically investigated for non-freezing injuries and are not
recommended [MilDerm].
629
Diet should have adequate protein. Smoking and other use of
tobacco products (or nicotine-containing aids to smoking cessation) are prohibited.
Treatment of posthyperemia is directed at rehabilitation, including physical therapy,
exercise, and surgical correction of deformities [
MilDerm].
630
C9.2.2.1.3. Disposition
The prognosis depends upon the extent of the original tissue damage, especially nerve
damage. Minimal and mild cases can resolve in hours to weeks and most eventually return to full
duty. However, more severe cases can take months to heal, may require surgery, and victims
may not be able return to full duty.
Military personnel who have previously suffered trench foot injury may be at increased
risk for future cold injury [PMID: 1969264].
631
C9.2.3. Vibration White Finger
Occupational cold exposure may be a contributing factor in the development of vibration
white finger [PMID: 8022312].
632
Workers should have adequate hand protection when handling
cold objects (see Contact and Handling of Cold Objects, above).
C9.2.4. Raynaud’s Phenomenon
Raynaud’s Phenomenon is “sensitivity of the hands and fingers to cold, as a result of
spasm of the digital arteries, with blanching and numbness or pain of the fingers” [Stedman’s].
633
It manifests as “episodic vasospastic ischemia of the digits . . . characterized by digital
blanching, cyanosis, and rubor after cold exposure and rewarming” [SAM-CD].
634
Low blood
pressure may be a risk factor for Raynaud’s Phenomenon [Creager].
635
As noted in the section on
vibration white finger (above), workers should have adequate hand protection when handling
cold objects (see Contact and Handling of Cold Objects, above). Workers with Raynaud’s
Phenomenon must be especially careful to use adequate gloving; under certain cold exposure
conditions, some such individuals may not be able to work safely.
C9.2.5. Cold Agglutinin Disease
Cold agglutinin disease is discussed
above. Exposure to cold stress (even without being
extreme) may precipitate or exacerbate symptoms. The post-infectious variant is usually mild
and self-limited and requires no specific management. However, patients with the idiopathic
variety who have acral symptoms must either move to a warmer climate or keep their ears, nose,
hands, and feet covered during cold weather [Schrier].
636
C9.2.6. Paroxysmal Cold Hemoglobinuria
Paroxysmal cold hemoglobinuria is a rare disorder involving cold-induced signs and
symptoms of intravascular hemolysis. Like cold agglutinin disease, it may present as a hemolytic
anemia. Episodic hemoglobinuria provoked by cold is reported [PMID: 2046431].
637
Paroxysmal
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
70
cold hemoglobinuria may be associated with viral infections, non-Hodgkin's lymphoma, or
syphilis [Schrier].
638
C9.3. Ocular (Eye) injuries Due to Cold Exposure
C9.3.1. Snow Blindness (Acute Photokeratitis, Solar Keratitis)
Snow blindness is said to be the most common acute ocular effect of environmental
ultraviolet (UV) radiation [
PMID: 9894351].
639
It is caused by exposure of the cornea to ultra-
violet radiation, often in snow conditions. It is similar in mechanism, treatment, and course to
“flash burns” caused by ultraviolet light given off during welding. Symptoms are eye pain and
photophobia, and may include tearing, conjunctival injection (redness), swollen eyelids, foreign
body sensation (a “gritty” feeling in the eyes), blurred vision, and headache. Chronic exposure
(decades or more) to ultraviolet radiation may cause spheroidal degeneration (Labrador
keratopathy) [PMID: 7236572,
640
PMID: 3778857],
641
and may lead to blindness [PMID:
6478308].
642
Treatment with a short-acting cycloplegic drop (e.g., cyclopentolate 1% or 2%, or
tropicamide 0.5% or 1%, or scopolamine 0.25%, to relieve painful ciliary spasm) and a topical
anesthetic given by the health care provider should be adequate for immediate pain relief. (Potent
topical anesthetics, such as proparacaine, should not be prescribed for, or sent home with, the
patient.) Topical antibiotic solution, suspension, or ointment (erythromycin, bacitracin,
trimethoprim / polymyxin, tobramycin, or gentamicin) may help prevent infection. Nonsteroidal
anti-inflammatory drugs (NSAIDs, such as ibuprofen) and small amounts of oral narcotic
analgesics may be used for pain control. Topical ophthalmic NSAIDs (e.g., diclofenac, ketorolac
tromethamine 0.5%) may be useful for pain relief [PMID: 12514694].
643
Commercially available UV-protective eye drops have not been found to offer adequate
protection against solar UV radiation under realistic conditions [PMID: 9704331].
644
C9.3.2. Cold Keratopathy (Corneal Epithelial Cold injury)
Cold keratopathy is a superficial cold injury of the corneal epithelium. It is commonly
found in cross-country skiers competing for long distances in cold weather (e.g., 9.3 miles in
3.2° F or -16° C). More severe cases may cause transient blurred vision. The apparent
mechanism of injury is cold exposure (rather than ultraviolet light exposure) of the lower cornea
due to incomplete closure of the eyelids. Cases may show punctate red staining (after instillation
of Rose-Bengal) of the lower cornea. Contact lenses may help prevent such injury. Spontaneous
healing within 24 hours is expected.
645
Figure 8 - Corneal Staining in Cold Keratopathy
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
71
Redrawn from Kolstad A, Opsahl R Jr. Cold injury to corneal epithelium. A cause of blurred vision in cross-country
skiers. Acta Ophthalmol (Copenh). 1969;47(3):656-9.
C9.3.3. Corneal Frostbite
Corneal frostbite is a serious ocular injury. It is generally caused only by exposure to
extreme cold (e.g., liquid nitrogen splashed in the eye) or by environmental cold exposure
involving loss of consciousness, defect of the eyelid, or other condition causing diminished
ability to protect the eye. It may result in loss of vision.
Initial care includes treating or preventing hypothermia; rewarming must avoid water,
saline, or air temperatures above 100.4° F (38° C). As the protection normally given by the
eyelid may be compromised, care should be taken to maintain hydration of the cornea and to
prevent trauma. Artificial tears without mercurial or benzalkonium antibacterial additives should
be used every 15 minutes or more frequently; if artificial tears are unavailable, sterile normal
saline may be substituted. Eye shields may be used. Do not patch (i.e., avoid anything touching
the cornea). Topical antibiotic solution (not ointment) should be given (e.g., erythromycin or
tobramycin) if there will be delay in ophthalmology evaluation. Definitive treatment by an
ophthalmologist should be sought.
C9.4. Hypothermia
Whereas exposure of the extremities or limited areas of skin may cause localized cold
stress injuries, exposure of the whole body, or significant portions of the body, to uncompensable
cold stress may cause hypothermia. Although hypothermia has been defined as “body
temperature significantly below 98.6°F (37°C)” [Dorland],
646
a more specific definition of
hypothermia applicable to clinical practice is the unintentional lowering of body core
temperature below 95.0
º
F (35.0
º
C) [CDC].
647
Although hypothermia is a serious cold stress
injury, lowered body temperature has limited application in certain medical procedures and
treatments. For example, in addition to use during cardiac surgery and neurosurgery, clinical and
experimental evidence has suggested hypothermia as an effective therapeutic adjunct in the
treatment of decompression sickness [PMID: 7187221].
648
C9.4.1. Public Health Impact of Hypothermia
During 1979 to 1998, approximately 700 persons (range 420 to 1,024) died annually in
the United States from hypothermia [
CDC].
649
During 1999, exposure to excessive natural cold
(ICD-10 code X31) was listed as the underlying cause of death for 598 persons in the United
States, and hypothermia (ICD-10 code T68) was listed as an injury that occurred to the decedent
in 1,139 deaths.
In 1994, excessive cold was reported as the reason for hospitalization for 30 men (27
Army and 3 Air Force) and 14 women (Army) [AMSUS].
650
The male to female hypothermia
ratio is 2.8 to 1 for the U.S. population [
MMWR].
651
Hypothermia is not limited to individuals outdoors during excessively cold conditions.
Only approximately half of deaths from hypothermia were attributed to extremely cold weather
[
CDC].
652
The CDC states that hypothermic mortality is underreported, because its physical
signs resemble other conditions and may not be recognized, hospitals may not use low-
temperature thermometers, medical personnel may be unaware of hypothermia's significance,
and an autopsy cannot prove hypothermia as an underlying cause of death [MMWR].
653
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
72
C9.4.2. Symptoms and Signs of Hypothermia
Individuals may not reliably assess whether they are experiencing hypothermia,
especially under certain conditions (e.g., during immersion) [PMID: 2803163,
654
PMID:
3795105].
655
Symptoms of hypothermia begin subtly with fatigue and loss of concentration
[
PMID: 1901977].
656
Ataxia, impaired judgment, oliguria, and slight confusion may be subtle
symptoms [PMID: 12092964],
657
but may progress to stupor, coma, and resemble rigor mortis
[PMID: 1901977].
658
The differential diagnosis in older adults includes cognitive decline,
cerebral vascular accident, hypothyroidism, or myxedema coma [PMID: 10024873].
659
The most
important differential diagnosis is death; patients who are cold and could be resuscitated must be
differentiated from patients who are cold because they are dead [PMID: 10994374].
660
In addition to decreased body temperature, neonatal hypothermia signs are lethargy,
refusal to feed, coldness to touch, cyanosis, apnea, and pedal edema [PMID: 10957833].
661
Hypothermia shifts the oxyhemoglobin-dissociation curve to the left, resulting in
decreased oxygen delivery to tissue [
PMID: 16730,
662
PMID: 9239580,
663
PMID: 7984198].
664
A review article estimated a hematocrit increase of 2 percent for every 1.8° F (1° C) decline in
temperature [
PMID: 7984198].
665
As in heat stress, EKG changes may be seen in hypothermia (see Figure 3 - J Wave
Appearance on Electrocardiogram).One investigation of 59 cases of hypothermia reported QT
inverval (adjusted for heart rate) prolongation in over 70 percent of patients, and bradycardia, J
wave, and T wave changes in approximately 50 percent of hypothermic patients; an inverse and
significant correlation between J wave voltage and core temperature was noted [PMID:
17027018].
666
C9.4.3. Classification of Hypothermia
Hypothermia may be classified as mild (90.0° F to 95.0° F, or 32.2° C to 35.0° C),
moderate (82.5° F to <90.0° F, or 28.0° C to <32.2° C), or severe (<82.5° F, or <28.0° C)
[CDC].
667
The cut-off temperatures for the various categories are not universally agreed upon in
the literature, but they are within what would be expected with different (Fahrenheit and Celsius)
systems in use. For example, a German article categorizes hypothermia as mild (89.6°F to 95°F,
or 32°C to 35°C), moderate (82.4°F to 89.6°F, or 28°C to 32°C), or severe (less than 82.4°F, or
28°C) [
PMID: 1882213].
668
At least one author has added another category: extreme (“body
temperature below 18-20 degrees C; no recordable EEG activity”) [PMID: 8236180].
669
Severity Fahrenheit Core
Temperature
Celsius Core
Temperature
Mild 90.0° to 95.0° 32.2° to 35.0°
Moderate 82.5° to < 90.0° 28.0° to < 32.2°
Severe < 82.5° < 28.0°
Table 12 - Classification of Hypothermia
Hypothermia may be thought of as primary (due to cold exposure) or secondary (related
to underlying or predisposing health-related conditions, such as illness, injury, intoxication or
extremes of age), and acute (due to cold exposure of less than 6 hours' duration) or chronic (due
to cold exposure of greater than 6 hours' duration) [Currier].
670
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
73
C9.4.4. Survival of Hypothermia
A study of survival of hypothermia found that negative survival factors are asphyxia,
with an odds ratio (OR) of 30, invasive rewarming methods (OR 20), slow rate of cooling (OR
10), asystole on arrival (OR 9), pulmonary edema or adult respiratory distress syndrome (ARDS)
during hospitalization (OR 8), elevated serum potassium (OR 2 / millimole / liter) and age (OR
1.03/year); positive survival factors are rapid cooling rate (OR 10), presence of ventricular
fibrillation in cardiac arrest patients (OR 9) and presence of narcotics and/or alcohol during
hypothermia (OR 5) [PMID: 1882213].
671
Factor Odds Ratio
For (+) or
Against (-)
Survival
Asphyxia
30 -
Invasive rewarming methods
20 -
Slow rate of cooling
10 -
Asystole on arrival
9 -
Pulmonary edema or ARDS
8 -
Elevated serum potassium (OR given per millimole per
liter)
2 -
Age (OR given per year)
1.03 -
Presence of narcotics and/or alcohol during hypothermia
5 +
Presence of ventricular fibrillation in cardiac arrest patients
9 +
Rapid cooling rate
10 +
Based on Locher T, Walpoth B, Pfluger D, Althaus U. Accidental hypothermia in Switzerland (1980-1987)--
case reports and prognostic factors. [German]. Schweiz Med Wochenschr. 1991 Jul 9;121(27-28):1020-8.
Table 13 - Hypothermia Survival Factors
Survival has been reported with a core temperature as low as 58.1° F (14.5° C) in a child
[PMID: 8601876].
672
Shock, requiring treatment with vasoactive drugs, is an independent risk
factor for mortality, while initial core temperature is not [
PMID: 11742934].
673
Hyperkalemia
may be a useful diagnostic tool in discerning dead from hypothermic victims [
PMID:
10994374].
674
In urban adult victims of hypothermia, decreased rates of rewarming were
associated with increased mortality and infection; rewarming rates seemed to reflect intrinsic
capacity for thermogenesis (i.e., hypothermic patients with underlying infection took longer to
rewarm and were less likely to survive) [
PMID: 16946289].
675
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
74
Organ System
Stage of
Hypothermia
Central
Nervous
System
Cardio-
vascular
Respiratory Dermato-
logic/Neuro-
muscular
Renal/
Gastro-
intestinal
Mild
(Excitation
Phase)
Apathy
Hyperreflexia
Disorientation
Tachycardia
Hypertension
Increased cardiac
output
Tachypnea
Bronchorrhea
Bronchospasm
Shivering
Vasoconstriction
Increased tone
Cold-induced
diuresis
Decreased GI
motility
Constipation
Moderate
(Slowing
Phase)
EEG
abnormalities
Hyporeflexia
Paradoxical
undressing
Bradycardia
Hypotension
Increased atrial
arrhythmias
Bradypnea
Diminished gag
Decreased O2
consumption
Decreased
shivering
Spasm
Ileus
GI erosions
Hepatic necrosis/
pancreatitis
Severe
Coma
Areflexia
EEG flattening
Asystole
Ventricular
arrhythmias
Pulmonary
edema
Apnea
Rigidity
Compartment
syndrome
Oliguria
Decreased renal
blood flow
Reproduced from Chang AK. Chapter 351 hypothermia. In Harwood-Nuss' Clinical Practice of Emergency Medicine. Wolfson AB,
Hendey GW, Hendry PL, Linden CH, Rosen CL, Schaider J; Sharieff GQ, Suchard JR, eds. 4th Edition. Copyright © 2005 Lippincott
Williams & Wilkins, Philadelphia. Used with permission.
Table 14 - Physiologic Changes During Hypothermia
C9.4.5. Predisposing Factors for Hypothermia
Decreased Heat
Production
Increased Heat
Loss
Hypothalamic
Dysfunction
Iatrogenic Cooling
CNS depression
(metabolic or
traumatic)
Immobility (age,
neuromuscular
disorders)
Endocrine failure
(adrenal /
pituitary /
thyroid)
Hypoglycemia /
malnutrition
Environmental
exposure
(inadequate
clothing or
shelter, wind
chill, low
humidity,
perspiration, wet
clothing)
Exfoliative skin
disease
Drugs / alcohol
Neuropathy
Sepsis
Shock
Burns
Acidosis / anoxia
CNS hemorrhage /
infarction
Drugs (e.g.,
phenothiazines)
Encephalopathy
Multiple
sclerosis
676,677
Poisoning (e.g.,
maneb)
678
Previous Head
Injury
679
Prior Cold Injury
Use of large
volumes of cool
fluids (<95° F or
35° C) for lavage
or IV
administration
Overly aggressive
treatment of
hyperthermia
(“overshoot”)
Adapted from Chang AK. Chapter 351 hypothermia. In Harwood-Nuss' Clinical Practice of Emergency Medicine.
Wolfson AB, Hendey GW, Hendry PL, Linden CH, Rosen CL, Schaider J; Sharieff GQ, Suchard JR, eds. 4th Edition. Copyright ©
2005 Lippincott Williams & Wilkins, Philadelphia. Used with permission.
Table 15 - Predisposing Factors in Hypothermia
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
75
Hypothalamic dysfunction and decreased ability to seek shelter from the cold also may
contribute. Sepsis, endocrine dysfunction (diabetic ketoacidosis, hypoglycemia, hypothyroidism,
hypopituitarism, hypoadrenalism), central nervous system (CNS) disorders (stroke, brain tumors,
spinal cord injury), and skin conditions (burns, erythroderma, psoriasis, ichthyosis) are additional
predisposing factors [Currier].
680
Underlying predisposing causes of hypothermia are diabetic ketoacidosis,
cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency,
malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction,
poly-pharmacy, and the use of sedative and narcotic drugs [
PMID: 11759373].
681
History of
orthostatic hypotension is a risk factor for developing accidental hypothermia [
PMID:
4065579].
682
Hypothermia subsequent to chemotherapy for Hodgkin's disease with
paraneoplastic fever has been reported [PMID: 17240740].
683
C9.4.5.1. Ethanol and Medications
Ethanol and drug use may increase heat loss due to cutaneous vasodilatation and
impaired shivering; substance abuse may also affect behavior so as to increase cold exposure
(see Alcohol, above).
Pyridostigmine bromide (30 mg) had no significant effect on physiologic responses to
cold-water immersion, but limited cold tolerance because of marked abdominal cramping
[PMID: 1938714].
684
Nitrous oxide (30%) has been shown to blunt the metabolic and shivering
responses to cold-water immersion [PMID: 1550280].
685
Triazolam has been found not to
significantly affect heat production or core temperature during cold-water immersion [PMID:
7575314].
686
Naphazoline 0.05-0.1% nasal decongestion solution has been reported as a cause of
hypothermia in children [PMID: 8067910].
687
Hypothermia may be due to nerve agent (sarin) exposure [PMID: 12387297].
688
C9.4.5.2. Clothing
Due to wearing heavy clothing, in extremely cold conditions there may be sweating and
discomfort of the torso from warmth during heavy work. Conversely, in spite of heavy clothing,
cold-induced numbness and pain of the face, hands, and feet is common [PMID: 3769908].
689
A
recent review, including simulation modeling, of the military Extreme Cold Weather Clothing
System during cold stress exposure reported that:
• Nuclear, biological, and chemical (NBC) protective clothing may inadequately protect
against hand and finger cooling, especially during rest following strenuous activity;
• There is no evidence substantiating suggestions that wearing NBC protective masks increases
susceptibility to facial frostbite;
• Any increased risk of hypothermia associated with wearing NBC protective clothing while
working in the cold is unlikely;
• Wearing NBC protective clothing during strenuous activity in cold weather may increase the
risk of hyperthermia, and cause sweat accumulation in clothing which may compromise
insulation and increase the risk of hypothermia during subsequent periods of inactivity
[
PMID: 10685594].
690
C9.4.6. Treatment of Hypothermia
Rapid core rewarming, airway control, and prolonged cardiopulmonary resuscitation
have been noted to be key factors in managing the hypothermic patient [PMID: 8121213].
691
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
76
Medical management of the older patient with moderate to severe hypothermia may require in-
hospital intensive care [PMID: 10024873].
692
Treatment should take into account not only the
degree of hypothermia, but also exposure time, state of consciousness, and complicating factors
such as trauma, drugs, or alcohol [
PMID: 8236180].
693
C9.4.6.1. Rewarming Methods
The method used to rewarm a patient with severe accidental hypothermia should be
adjusted to the hemodynamic status [PMID: 8719198].
694
Of conventional rewarming methods, trunk immersion has been found to have the
smallest afterdrop (see
below), shortest recovery period, and most rapid rewarming [PMID:
7417132].
695
One article reported that surface and conventional core rewarming methods result
in an average temperature increase of 4.3° F (2.4° C) per hour [PMID: 3729178];
696
however, it
has been claimed that immersion rewarming can increase cardiac temperature at least twice as
fast as inhalation rewarming, and inhalation rewarming may increase cardiac (i.e., body core)
temperature twice as fast as spontaneous rewarming [
PMID: 6322264].
697
When hypothermia is
associated with cardiac arrest, rewarming by extracorporeal support is recommended (see
below)
[PMID: 8236180].
698
Inhalation rewarming of mild (body core temperature of 95° F or 35° C) hypothermia
with heated, humidified oxygen may be as effective as rewarming by immersion in a hot bath
[PMID: 1180782].
699
However, one study found no benefit from pre-hospital inhalation and
peripheral rewarming for the treatment of mild hypothermia [PMID: 1854075].
700
In more severe hypothermia, inhalation therapy is the recommended treatment in the field
[PMID: 7417132].
701
Evaluation of rewarming techniques shows that results from forced air
rewarming are equivalent to or better than results from invasive rewarming methods, except for
rewarming with cardiopulmonary bypass [PMID: 11107727].
702
Severe hypothermia has been
managed with warm IV fluids, peritoneal dialysis with warm fluids [PMID: 8698555],
703
and
hemodialysis with an average rise of 3.4° F/hour (1.9° C/hour) [PMID: 11479182].
704
C9.4.6.2. Afterdrop
Afterdrop is a phenomenon of conductive heat loss. Afterdrop refers to a continued
decrease in measured body temperature after removal from cold stress exposure. In one study,
surface to volume ratio and body mass index predicted afterdrop duration [
PMID: 11043627].
705
Afterdrop and hypothermia can occur commonly after recreational cool-water swimming, and
some researchers suggest that participants should be observed for signs of temperature decrease
following removal from cold stress [PMID: 11043627].
706
Afterdrop of core temperature, ventricular fibrillation precipitated by rough handling,
hypovolemia, or fluid overload all have been noted as potential contributors to hypothermia
deaths [PMID: 1483774].
707
C9.4.6.3. Extreme Cases of Hypothermia
C9.4.6.3.1. Cardiopulmonary Bypass
Cardiopulmonary bypass for core rewarming allows circulatory support while avoiding
myocardial damage from prolonged external cardiac massage, rapidly increases the myocardial
temperature, counteracts myocardial temperature gradients so that direct current cardioversion is
successful, avoids "rewarming shock," and improves microcirculatory flow [PMID: 3729178].
708
Immediate cardiopulmonary bypass for rewarming is recommended for patients in ventricular
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
77
fibrillation with core temperatures below 86° F (30° C) [PMID: 3729178]
709
who have no
documented contraindications to resuscitation [PMID: 7984198].
710
Femoral flow rates of 2 to 7
liters per minute may be used in cardiopulmonary bypass rewarming [Long].
711
One review
noted that with the warmer set at 100.4° to 104° F (38° to 40° C), core temperature will rise at
1.8° to 3.6° F (1° to 2° C) every 3 to 5 minutes [PMID: 7984198].
712
C9.4.6.3.2. Bretylium
Bretylium, no longer generally recommended for treatment of ventricular fibrillation
[AHA],
713
has been found to increase the threshold for ventricular fibrillation in dogs if
administered prior to hypothermia [
PMID: 1616517].
714
However, resuscitation of hypothermic
dogs in ventricular fibrillation using bretylium was no more effective than using saline [
PMID:
6486552].
715
Bretylium may be of value for prevention of ventricular fibrillation in hypothermia
during rewarming; some clinicians think it should be considered a first-line agent for treatment
of ventricular fibrillation in hypothermia [Currier].
716
Extremely aggressive measures, including median sternotomy with cardiopulmonary
bypass, have been advocated to rewarm pediatric victims of cold-water submersion who suffer
severe hypothermia (<82.4° F or 28° C) and cardiac arrest (asystole or ventricular fibrillation)
[PMID: 11886730].
717
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
78
Figure 9 - Hypothermia Treatment Algorithm
C9.4.6.3.3. Triage
In multiple-victim situations, triage may be essential to allocate limited resources (e.g.,
cardiopulmonary bypass equipment). A study of avalanche victims (in whom asystole is
generally due to asphyxia and not primarily to hypothermia [
PMID: 8701103])
718
found that
plasma potassium (greater than 9 millimoles per liter), pH (equal to or less than 6.50) or an
activated clotting time (exceeding 400 seconds) may identify hypothermic arrest victims in
whom death preceded cooling (and thus have no chance of resuscitation after rewarming)
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
79
[PMID: 8191027].
719
Another study suggested potassium of 10 millimoles per liter as a cut-off
[PMID: 8701103].
720
However, there is no variable that can with certainty predict successful
resuscitation efforts [PMID: 10925611].
721
C9.4.6.3.4. Potential Complications
Serious complications of hypothermia include hemorrhagic pancreatitis, lung edema and
myxomatous skin edema [
PMID: 10998830].
722
Survivors of neonatal hypothermia may show severe developmental delay, with abnormal
cerebral computed tomography findings, including diffuse cerebral edema, with reversal of the
normal density relationship between grey and white matter and a relative increased density of the
thalami, brainstem and cerebellum (the “reversal sign”), cerebral atrophy, and multicystic
encephalomalacia [PMID: 9634453].
723
Acutely, intracranial pressure monitoring may be
important in pediatric victims, especially those who survive drowning [PMID: 3550722].
724
Mild perioperative hypothermia is significantly associated with infection of surgical
wounds [PMID: 11395189].
725
In one report, all 4 surviving victims of hypothermia treated with
cardiopulmonary bypass developed temporary pulmonary problems, and 2 developed wound
infections; average hospital stay was 21 days [PMID: 3729178].
726
C9.4.7. Follow-up of Hypothermia
Follow-up of hypothermia victims may include neuropsychiatric testing and brain
imaging studies. Magnetic resonance imaging showed cerebellar atrophy in one patient that
received rewarming with cardiopulmonary bypass with mild clinical signs [PMID: 9366581].
727
C9.4.8. Prognosis in Hypothermia
The prognosis is excellent in patients in whom no hypoxic event precedes hypothermia
and no serious underlying disease exists [PMID: 8719198].
728
Out of a group of 32 victims, age 15 to 36 years, of severe hypothermia (core temperature
less than 82.4° F or 28° C, with circulatory arrest) that received rewarming with
cardiopulmonary bypass, 15 survived. Follow-up for over 5 years of survivors showed
neurological and neuropsychological deficits observed in the early period after rewarming had
fully or almost completely disappeared. Investigators concluded that that young, otherwise
healthy people can survive accidental deep hypothermia with no or minimal cerebral impairment,
even with prolonged circulatory arrest, and that cardiopulmonary bypass appears to be an
efficacious rewarming technique [
PMID: 9366581].
729
C9.4.8.1. Predicting Outcome in Hypothermia
In one report, emergency room Glasgow coma score and trauma score were not indicative
of outcome of victims of hypothermia [
PMID: 3202789].
730
C9.4.8.2. Elderly Victims
In a series of hypothermia victims aged over 65 years, of those who survived the index
admission, the 3-year mortality was 100% in those with primary hypothermia and 24% in those
with secondary hypothermia [
PMID: 3577949].
731
C9.4.8.3. Pediatric Victims
In neonates with a birth weight of less than 700 gm, hypothermia is a factor correlating
with non-survival [PMID: 6463697].
732
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
80
Of 12 survivors of infant hypothermia, by ages 3 to 12 years, one had mild and one had
severe psychomotor retardation (both of the latter victims had sepsis on first admission for
hypothermia). All hypothermic infants without sepsis had normal developmental achievements
[
PMID: 10663286].
733
An 8 year old child treated aggressively with open rewarming and
resuscitation by thoracotomy and pleural lavage for cardiac arrest with core temperature 77° F
(25° C) recovered without any postoperative complications; follow-up at two years showed some
neuropsychological defects [
PMID: 7857072].
734
Figure 10 - Assessment (Category) of Cold Injury
C9.5. Prevention of Further Heat Stress injuries in the Population
When a cold stress injury is recognized, steps should be taken to prevent others in the
involved population from cold stress injury. The victim may serve as a sentinel event, alerting
health care workers, safety, and supervisors to the existence of a cold-related health risk.
Training (or retraining) on cold stress injuries may be appropriate (see
OPNAV 5100.23
series).
735
A check of environmental thermometers or WBGT equipment should be done, if it is
possible that faulty equipment may have contributed to the cold stress injury. Adequacy of
clothing and heating facilities (HVAC system, if present) should be verified. With appropriate
measures, most cold stress-related injuries can be prevented.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
81
Chapter 10:
C10. Reporting
All cold stress-related injuries should be reported through the Naval Disease Reporting
System. A simultaneous report to the Naval Safety Center should be made using the Web
Enabled Safety System (WESS). Marine Corps heat injuries should be reported in accordance
with MCO P5102.1A (which prescribes the mandatory use of electronic mishap reporting of all
Marine Corps ground mishaps to the Marine Corps database maintained at the Naval Safety
Center) and BUMEDINST 6220.12A (which stipulates Naval Disease Reporting System
electronic report, or written, fax, e-mail or phone report to the cognizant
NAVENPVNTMEDU).
736
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
82
Chapter 11:
C11. Heat Stress Injuries Prevention and Treatment
C11.1. Prevention of Heat injuries
Heat stress is commonly encountered in military operations, and may cause injury or
death, resulting in decreased readiness. Most heat stress injuries are preventable.
The body constantly generates heat; activity (work or exercise) generates more heat. The
body cools itself in heat stress conditions primarily by sweating.
Risk factors and conditions that predispose to heat stress injuries include high humidity,
little air movement (wind), overhead sun, elevation below sea level, sunburn or other skin
condition, clothing or gear that hinders skin “breathing,” illness, recent immunizations, prior heat
injury, recent heat stress exposure, age (very young or very old), lack of acclimatization (not
taking a few weeks to “get used to” heat stress), dehydration, medications, substance abuse,
fatigue, high activity level, elevated body mass (being overweight, whether obese or very
muscular), and being around very hot objects (e.g., hot steel).
Preventive measures against heat stress injury are focused on limiting exposure to heat
stress (by decreasing activity or avoiding hot environments), acclimatization (taking 3 weeks to
gradually get used to the heat), maintaining adequate hydration and limiting strenuous activity.
Water, electrolyte solutions (sports drinks), or even carbonated beverages may be used to replace
fluids lost through sweating. “Forced drinking” (i.e., drinking even though not thirsty) during
activity in heat stress should be done, as thirst lags behind actual need for water. Water intake
should not exceed 1.5 quarts per hour and no more than 12 quarts per day (note: highly
conditioned personnel may require even more water than that, and for such people water intake
should not be limited; however, 12 quarts per day is very much and is not often required).
Activity is controlled by observing work-rest cycles, established based on the wet bulb globe
temperature index (WBGT). A specific instrument measures the WBGT; the WBGT is not the
same as the temperature in the sun or shade, the “heat index,” or other reading given by weather
stations.
Symptoms (feelings of being overheated or of chills) and signs of impending heat stroke
(confusion, incoordination, decreased sweating, “gooseflesh”) should be closely followed.
Checking body temperature can be done using oral (mouth) thermometers (provided the person
has not had hot food or water for 5 minutes and cold food or water for 30 minutes, and can avoid
mouth breathing) or ear probes (provided no water has splashed in the ear, and cold or hot air is
not blowing into the ear); core temperature may be determined with a rectal thermometer, but
accuracy is best with an esophageal thermometer.
Heat injuries may be generally classified as minor (miliaria, heat syncope, heat edema,
heat tetany, heat cramps) and major (heat exhaustion, heat stroke). Minor heat injuries generally
do not cause permanent injury, but may diminish operational readiness. Major heat injuries have
the potential to cause permanent injury or death.
Heat injuries often do not fall into distinct categories. A case of heat injury may exhibit
signs and symptoms from more than one diagnosis. Also, a heat injury may progress from mild
(for example, heat cramps) to severe (heat exhaustion or even heat stroke) if adequate treatment
is not given in a timely manner. Severe heat illness, such as heat stroke, does not have to be a
linear progression through various heat illnesses, but can be sudden and explosive.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
83
C11.1.1. Minor Heat Injuries
C11.1.1.1. Miliaria
Heat stress may cause miliaria (“heat rash”), an inflammatory skin reaction characterized
by redness, with papules and vesicles at sweat glands. Miliaria can impair sweating and reduce
heat tolerance. Treatment is removal from heat stress exposure. Application of cool wet cloths,
cool starch baths, calamine lotion, and corticosteroid lotion with or without 0.25% menthol may
alleviate symptoms. Antihistamines may inhibit sweating, and should be limited to use for severe
itching in air conditioning.
C11.1.1.2. Heat Syncope
Heat syncope (fainting), if present, occurs during the first 5 days of heat exposure, due to
vascular insufficiency (low blood pressure). Symptoms are syncope and postural
lightheadedness. Victims are tachycardic (rapid pulse), have normal temperatures, are sweating,
and have postural hypotension. Treatment is supine position, elevation of the feet, and oral
fluids.
C11.1.1.3. Heat Edema
Heat edema is lower extremity edema (swelling) that develops or worsens soon after heat
stress exposure (usually within 48 hours). No specific treatment is required, and the condition is
expected to resolve with continued acclimatization. In more severe cases, diuretics may be given
to enable victims to complete heat acclimatization.
C11.1.1.4. Heat Tetany
Heat tetany is due to hyperventilation after being exposed to heat stress, usually prior to
acclimatization. Symptoms include muscle spasm (local or generalized) and numbness and
tingling around the mouth. Blood is alkaline and may show hypocarbia. Treatment is temporary
removal from heat stress.
C11.1.1.5. Heat Cramps
Heat cramps occur in heat-acclimatized individuals exercising or working in heat stress
conditions, especially when continued over several days. Heat cramps are thought to be from
hyponatremia (low sodium). Other than muscle cramps (and possibly fatigue), victims generally
feel well. Treatment is increased dietary sodium intake.
C11.1.2. Major Heat Injuries
C11.1.2.1. Heat Exhaustion
Heat exhaustion is a major heat stress-related injury, and may be a precursor to heat
stroke. It is an inability to sustain required cardiac output. There are two types of heat
exhaustion: sodium (salt) depletion and water depletion (dehydration or anhydrotic).
Sodium-depletion heat exhaustion is from exposure to excessive heat stress while
consuming sufficient water but insufficient salt. Symptoms are nausea, vomiting, diarrhea,
weakness, alterations of mental status, and minimal or no thirst. The victim usually has cool,
moist skin that may be sticky and pale. (NOTE: SKIN FINDINGS IN HEAT INJURIES MAY
NOT BE CONSISTENT!) The victim often is hypotensive (low blood pressure) and tachycardic
with normal body temperature and normal urine volume. Hyponatremia (serum sodium less than
130 mEq/L) always is present, and may result from inadequate dietary salt, excessive sodium
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
84
loss in sweat (more likely prior to heat acclimatization), or water intoxication (drinking too much
water). Treatment is removal of the victim to a cool place, removing heavy clothes, and
administration of sodium replacement (oral or IV fluids of normal tonicity, such as D5NS or
Lactated Ringer’s Solution) until symptoms clear and pulse and urine findings normalize
(including urine sodium content of at least 10 mEq/L). If sodium is very low (less than 120
mEq/L), sodium replacement must be monitored, as it may lead to cerebral edema if done too
rapidly. Avoid aspirin and other non-steroidal anti-inflammatory agents. Active cooling (see
Cooling, below) may be performed as needed.
Water-depletion heat exhaustion is from excessive heat stress without adequate water
replacement. Symptoms are malaise, vomiting, dizziness, confusion, anxiety, agitation,
weakness, fatigue, prostration, and even delirium and collapse. Victims are dehydrated and have
elevated temperatures (at least 100.4° F or 38° C). Hyperventilation, tetany, oliguria (low urine
output), and hypernatremia may be present. Heat stroke may be imminent. Treatment is removal
from heat, removal of heavy clothing, active cooling (aggressive cooling if necessary to maintain
core temperature less than 102° F or 38.9° C), and emergent transport to a hospital for water
replacement. IV fluids replacement should try to correct serum sodium at no more than 2 mEq/L
per hour.
C11.1.2.2. Heat Stroke
Heat stroke is a seriously elevated temperature (> 104° F or 40° C) that causes central
nervous system (CNS) injury. Heat stroke is a life-threatening heat stress exposure injury.
Symptoms and signs of heat stroke include feeling overheated, weakness, fatigue, diarrhea,
vomiting, irritability, bizarre behavior, euphoria, combativeness, hallucinations, loss of
consciousness, and coma. Sweating may or may not be present. Complications include
arrhythmias, shock, rhabdomyolysis (muscle breakdown), renal failure, liver failure, coagulation
abnormalities (include disseminated intravascular coagulation), adult respiratory distress
syndrome, and death. Treatment is immediate cooling (including removal of clothing) and
removal to a hospital (continuing cooling by maintaining ventilation). In addition to active and
aggressive cooling (see below), advanced cooling techniques (removal, cooling, and re-
introduction of blood) may be attempted. In addition to oxygen, NG intubation, and other general
supportive therapy, aggressive medical management is appropriate, possibly including
mechanical ventilation, blood purification therapy, and treatment of infections. After recovery,
re-exposure to heat stress conditions must be done with caution.
C11.2. Cooling
Active cooling may be done by fanning (anything from a fan to a helicopter downdraft,
with or without water or mist), cold or ice water immersion (with intermittent warm air exposure
or rubbing the skin to maintain skin blood flow), cold packs (ice packs or ice water slush),
cooling blankets (containing a circulating coolant), and cooled nasal air or oxygen. Aggressive
cooling may be done using ice water nasogastric (NG) lavage, ice water enemas, and iced
peritoneal lavage. While certain individuals may respond to such measures, cold water
immersion is considered to be the “gold standard” for rapid body cooling.
C11.3. Reporting Heat injuries
Heat stress injuries must be reported through the Naval Disease Reporting System and
simultaneously to the Naval Safety Center using the Web Enabled Safety System (WESS).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
85
Chapter 12:
C12. Cold Stress Injuries Prevention and Treatment
Cold stress exposure can decrease readiness by causing injury, illness, and death.
Predisposing factors to cold injuries are alcohol use, cold-water immersion, clothing that
is inadequate or wet, inadequate shelter, using skin lotions or oils as cold protection, handling
cold objects (especially metal), wind, high elevation (altitude), dehydration, inadequate rest, poor
nutrition, lack of acclimatization, motion sickness, high activity levels followed by rest (causing
sweating followed by chilling, as may occur through use of MOPP gear), not removing foot gear
and changing socks at least daily, and underlying vascular conditions (i.e., abnormal blood vessel
constriction, as may be present with previous cold-related injury, Raynaud’s phenomenon, etc.).
Associated injuries may include dehydration, ultraviolet eye or skin injury (sunburn),
chapped lips, slips and falls on ice, and high altitude-related conditions.
Most cold-related health consequences are preventable. Preventive measures include
ensuring adequate shelter and clothing (especially gear for the face, hands, feet, and head),
adequate nutrition and hydration, limiting or avoiding alcohol, gradual acclimatization (taking a
few weeks “to get used to the cold”), changing socks at least daily, using proper equipment (such
as dry suits for diving, anti-exposure suits on deck, and plastic-coated tools and equipment),
taking wind speed and precipitation into account, and exercising sound judgment in cold stress
conditions.
Superficial (skin) cold stress injury, such as chilblain, can result in discoloration or
scarring. Symptoms of chilblain are burning and itching red patches on the fingers and/or toes,
generally bilaterally and exacerbated by sunlight.
Cold stress injuries of acral areas (i.e., extremities, ears, nose), include trench foot and
frostbite, which can result in scarring, decreased function, or even loss of the affected body part.
Trench foot is a non-freezing cold injury of the feet. Symptoms of trench foot are cold,
numbness, paresthesias, itching, and painful weight bearing, progressing to anesthesia (“walking
on blocks of wood”). Signs include pallor, mottled purple coloration, swelling, and edema. After
rewarming, sensation returns with paresthesias, pain, and increased heat sensitivity. Blisters,
circulatory compromise, local hemorrhage, and ecchymosis may characterize severe cases,
which may have a prolonged post-inflammatory phase involving compromised blood supply.
Trench foot may result in a peripheral neuropathy.
Frostbite is a freezing injury, classified as first (superficial), second (full-thickness,
usually with clear blisters), third (skin and subcutaneous tissue, sometimes with hemorrhagic
blisters), and fourth degree (deeper structures, including tendons, muscles, and bone). Symptoms
range from pain (cold or burning sensation) to numbness. Signs of frostbite vary and include
white patches, diffuse redness, hardening or waxy appearance of the skin, mottled gray
coloration, tenderness, diminished light touch, and anesthesia. Determining depth of injury may
take days. Delineating tissue viability may take months; technetium bone scanning (bone
scintigraphy) may be used.
Whole-body cold stress can result in hypothermia, which, if severe or if not treated in
time, can result in organ damage or death.
Cold stress may also exacerbate or unmask underlying conditions, such as acrocyanosis,
rosacea, cold agglutinin disease, cold panniculitis, xerosis, cold-induced urticaria, vibration
white finger, Raynaud’s phenomenon, and paroxysmal cold hemoglobinuria. Persons with those
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
86
conditions should take extra precautions to wear adequate clothing and equipment, or avoid cold
stress exposure entirely.
Treatment of cold injuries is rewarming. Affected parts should be elevated. Use
(movement), weight-bearing, and rubbing should be avoided. Smoking is prohibited until
recovery is complete.
Chilblain and trench foot injuries are best rewarmed using air at room temperature.
Rewarming may be done even though re-exposure to cold is anticipated. Treatment of chilblain
may include nifedipine, thyrocalcitonin, and hemodilution.
Rewarming of frostbite should be delayed until the victim has been removed from risk of
re-exposure to the cold and can be kept at bed rest. Treatment of frostbite is rapid rewarming,
using immersion in water at or just above body temperature (no more than 108° F or 42.2° C).
Additional measures include IV fluids (to maintain hydration and circulation), dextran (to limit
edema), thrombolytics (fibrinolysin, streptokinase within 48 hours), anticoagulants (heparin),
anti-inflammatory agents (non-steroidals such as ibuprofen and aspirin), sympathetic blockade
(epidural bupivacaine or morphine), hyperbaric oxygen, debridement without anesthesia (i.e., to
avoid removing innervated, viable tissue), and delayed (60 to 90 days) surgical amputation, if
necessary. Prevention of infection should include tetanus toxoid booster, if required, and may
include adding mild antiseptics to whirlpool baths. Signs of infection, two-point discrimination,
vibration, and movement examinations should be followed closely during frostbite treatment.
Hypothermia treatment includes rapid core rewarming, airway control, and prolonged
cardiopulmonary resuscitation (if necessary). Heated, humidified oxygen (when available in the
field) may be used alone or in conjunction with or replaced by trunk immersion, warm IV fluids,
peritoneal dialysis with warm fluids, and hemodialysis. When hypothermia is associated with
hemodynamic instability (e.g., cardiac arrest), rewarming by extracorporeal support
(cardiopulmonary bypass) is recommended. Afterdrop (a continued decrease in core temperature
after removal from cold), ventricular fibrillation, hypovolemia, and fluid overload are potential
(and potentially deadly) complications of aggressive rewarming.
Cold stress injuries must be reported through the Naval Disease Reporting System and
simultaneously to the Naval Safety Center using the Web Enabled Safety System (WESS).
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
87
Chapter 13:
C13. References
1
Stolwijk JA. Heat exchangers between body and environment. Bibl Radiol. 1975;(6):144-50.
2
CHIPPM. TB MED 507 Department of the Army technical bulletin occupational and environmental health
prevention, treatment and control of heat injury. Headquarters, Departments of the Army, Navy and Air Force.
Washington, DC. 25 July 1980.
3
Kunimoto M, Kirno K, Elam M, Karlsson T, Wallin BG. Neuro-effector characteristics of sweat glands in the
human hand activated by irregular stimuli. Acta Physiol Scand. 1992 Oct;146(2):261-9.
4
Hasan W, Cowen T, Barnett PS, Elliot E, Coskeran P, Bouloux PM. The sweating apparatus in growth hormone
deficiency, following treatment with r-hGH and in acromegaly. Auton Neurosci. 2001 Jun 20;89(1-2):100-9.
5
Sneppen SB, Main KM, Juul A, Pedersen LM, Kristensen LO, Skakkebaek NE, Feldt-Rasmussen U. Sweat
secretion rates in growth hormone disorders. Clin Endocrinol (Oxf). 2000 Nov;53(5):601-8.
6
Main K, Nilsson KO, Skakkebaek NE. Influence of sex and growth hormone deficiency on sweating. Scand J Clin
Lab Invest. 1991 Sep;51(5):475-80.
7
Robertson MT, Boyajian MJ, Patterson K, Robertson WV. Modulation of the chloride concentration of human
sweat by prolactin. Endocrinology. 1986 Dec;119(6):2439-44.
8
Kaufman FL, Mills DE, Hughson RL, Peake GT. Effects of bromocriptine on sweat gland function during heat
acclimatization. Horm Res. 1988;29(1):31-8.
9
Kolka MA, Cadarette BS. Heat exchange after cholinolytic and oxime therapy in protective clothing. Mil Med.
1990 Sep;155(9):390-4.
10
Montain SJ, Latzka WA, Sawka MN. Fluid replacement recommendations for training in hot weather.
Mil Med. 1999 Jul;164(7):502-8.
11
Stephenson LA, Kolka MA. Thermoregulation in women. Exerc Sport Sci Rev. 1993;21:231-62.
12
Kondo N, Nishiyasu T, Ikegami H. The influence of exercise intensity on sweating efficiency of the whole body
in a mild thermal condition. Ergonomics. 1996 Feb;39(2):225-31.
13
Candas V, Libert JP, Vogt JJ. Experimental determination of coefficient of evaporative heat loss in still air
[French]. Eur J Appl Physiol Occup Physiol. 1975 Apr 4;34(2):97-108.
14
Roberts MF, Wenger CB. Control of skin circulation during exercise and heat stress. Med Sci Sports. 1979
Spring;11(1):36-41.
15
Stephenson LA, Kolka MA. Thermoregulation in women. Exerc Sport Sci Rev. 1993;21:231-62.
16
Boushel R, Langberg H, Green S, Skovgaard D, Bulow J, Kjaer M. Blood flow and oxygenation in peritendinous
tissue and calf muscle during dynamic exercise in humans. J Physiol. 2000 Apr 1;524 Pt 1:305-13.
17
Brengelmann GL, Johnson JM, Hermansen L, Rowell LB. Altered control of skin blood flow during exercise at
high internal temperatures. J Appl Physiol. 1977 Nov;43(5):790-4.
18
Kregel KC, Wall PT, Gisolfi CV. Peripheral vascular responses to hyperthermia in the rat. J Appl Physiol. 1988
Jun; 64(6): 2582-8.
19
Armstrong LE, Epstein Y. Fluid-electrolyte balance during labor and exercise: concepts and misconceptions. Int J
Sport Nutr. 1999 Mar;9(1):1-12.
20
Maughan RJ, Leiper JB, Shirreffs SM. Factors influencing the restoration of fluid and electrolyte balance after
exercise in the heat. Br J Sports Med. 1997 Sep;31(3):175-82.
21
Meyer LG, Horrigan DJ Jr, Lotz WG. Effects of three hydration beverages on exercise performance during 60
hours of heat exposure. Aviat Space Environ Med. 1995 Nov;66(11):1052-7.
22
Byrne C, Lim CL, Chew SA, Ming ET. Water versus carbohydrate-electrolyte fluid replacement during loaded
marching under heat stress. Mil Med. 2005 Aug;170(8):715-21.
23
Gatorade, P.O. Box 049003, Chicago, IL 60604-9003. Phone 800-884-2867.
24
CHIPPM. TB MED 507/AFPAM 48-152(I). Department of the Army Technical Bulletin Heat Stress Control and
Casualty Management. Headquarters, Department of the Army and Air Force. Washington, DC. 7 March 2003:28.
25
WHO. The treatment of diarrhoea a manual for physicians and other senior health workers. World Health
Organization WHO/CDR/95.3 10/95.
http://www.who.int/child-adolescent-
health/New_Publications/CHILD_HEALTH/textrev4.htm#ANNEX%202
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
88
26
Stokely-Van Camp, Inc. Gatorade our products your performance how we compare. Stokely-Van Camp, Inc. a
subsidiary of The Quaker Oats Company, a wholly-owned subsidiary of PepsiCo, Inc. 2002.
http://www.gatorade.com/products_perform/thirst_quench/compare.html
27
Kenefick RW, O'Moore KM, Mahood NV, Castellani JW. Rapid IV versus oral rehydration: responses to
subsequent exercise heat stress. Med Sci Sports Exerc. 2006 Dec;38(12):2125-31.
28
Mitchell JB, Costill DL, Houmard JA, Fink WJ, Robergs RA, Davis JA. Gastric emptying: influence of prolonged
exercise and carbohydrate concentration. Med Sci Sports Exerc. 1989 Jun;21(3):269-74.
29
Maughan RJ, Leiper JB, Shirreffs SM. Factors influencing the restoration of fluid and electrolyte balance after
exercise in the heat. Br J Sports Med. 1997 Sep;31(3):175-82.
30
Maughan RJ. Fluid and electrolyte loss and replacement in exercise. J Sports Sci. 1991 Summer;9 Spec No:117-
42.
31
Mitchell JB, Costill DL, Houmard JA, Fink WJ, Robergs RA, Davis JA. Gastric emptying: influence of prolonged
exercise and carbohydrate concentration. Med Sci Sports Exerc. 1989 Jun;21(3):269-74.
32
Marzio L, Formica P, Fabiani F, LaPenna D, Vecchiett L, Cuccurullo F. Influence of physical activity on gastric
emptying of liquids in normal human subjects. Am J Gastroenterol. 1991 Oct;86(10):1433-6.
33
Sawka MN, Montain SJ. Fluid and electrolyte supplementation for exercise heat stress. Am J Clin Nutr 2000
Aug;72(2 Suppl):564S-72S.
34
NEHC. Navy environmental health center technical manual NEHC-TM92-6 prevention and treatment of heat and
cold stress injuries. Navy Environmental Health Center, Bureau of Medicine and Surgery. June 1992.
35
Jorgensen R, ed. Fan Engineering 6
th
Edition An engineer’s handbook on air, its movement and distribution in air
conditioning, industrial ventilation, mechanical draft, conveying, and other applications employing fans. Buffalo
Forge Company. Buffalo. 1961:335.
36
National Weather Service Web site.
http://www.srh.noaa.gov/jan/hindex.html
37
Hoppe P. The physiological equivalent temperature - a universal index for the biometeorological assessment of
the thermal environment. Int J Biometeorol. 1999 Oct;43(2):71-5.
http://windchill-conference.ec.gc.ca/workshop/papers/pdf/session_1_paper_3_e.pdf
3838
Donoghue AM, Sinclair MJ, Bates GP. Heat exhaustion in a deep underground metalliferous mine. Occup
Environ Med. 2000 Mar;57(3):165-74.
39
Pandolf KB, Gange RW, Latzka WA, Blank IH, Kraning KK 2nd, Gonzalez RR. Human thermoregulatory
responses during heat exposure after artificially induced sunburn. Am J Physiol. 1992 Apr;262(4 Pt 2):R610-6.
40
McLellan TM, Pope JI, Cain JB, Cheung SS. Effects of metabolic rate and ambient vapour pressure on heat strain
in protective clothing. Eur J Appl Physiol Occup Physiol. 1996;74(6):518-27.
41
ACGIH Worldwide. 2003 TLVs and BEIs Threshold Limit Values for Chemical Substances and Physical Agents
& Biological Exposure Indices. American Conference of Governmental Industrial Hygienists, Cincinnati. 2003:173.
42
Jones JG. The physiological cost of wearing a disposable respirator. Am Ind Hyg Assoc J. 1991 Jun;52(6):219-25.
43
Kerle KK, Nishimura KD. Exertional collapse and sudden death associated with sickle cell trait.
Am Fam Physician. 1996 Jul;54(1):237-40.
44
Cui J, Arbab-Zadeh A, Prasad A, Durand S, Levine BD, Crandall CG. Effects of heat stress on thermoregulatory
responses in congestive heart failure patients. Circulation. 2005 Oct 11;112(15):2286-92.
45
Ohtsuka Y, Yabunaka N, Watanabe I, Noro H, Fujisawa H, Agishi Y.Thermal stress and diabetic complications.
Int J Biometeorol. 1995 Jan;38(2):57-9.
46
Franklin QJ. Sudden death after typhoid and Japanese encephalitis vaccination in a young male taking
pseudoephedrine. Mil Med. 1999 Feb;164(2):157-9.
47
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
48
Kark JA, Burr PQ, Wenger CB, Gastaldo E, Gardner JW. Exertional heat illness in Marine Corps recruit training.
Aviat Space Environ Med. 1996 Apr;67(4):354-60.
49
Wallace RF, Kriebel D, Punnett L, Wegman DH, Wenger CB, Gardner JW, Gonzalez RR. The effects of
continuous hot weather training on risk of exertional heat illness. Med Sci Sports Exerc. 2005 Jan;37(1):84-90.
50
Bergeron MF. Heat cramps during tennis: a case report. Int J Sport Nutr. 1996 Mar;6(1):62-8.
51
Sawka M. Telephone conversation with Muller J. 21 July 2004.
52
Havenith G, van Middendorp H. The relative influence of physical fitness, acclimatization state, anthropometric
measures and gender on individual reactions to heat stress. Eur J Appl Physiol Occup Physiol. 1990;61(5-6):419-27.
53
Garrow JS, Webster J. Quetelet's index (W/H2) as a measure of fatness. Int J Obes. 1985;9(2):147-53.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
89
54
CDC. BMI: body mass index body mass index formula. United States Department of Health and Human Services,
Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion,
Division of Nutrition and Physical Activity. April 29, 2002.
http://www.cdc.gov/nccdphp/dnpa/bmi/bmi-adult-formula.htm
55
CDC. Body Mass Index Web Calculator. United States Department of Health and Human Services, Centers for
Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Division of
Nutrition and Physical Activity. July 24, 2002.
http://www.cdc.gov/nccdphp/dnpa/bmi/calc-bmi.htm
56
Cooper JK. Preventing heat injury: military versus civilian perspective. Mil Med. 1997 Jan;162(1):55-8.
57
Krueger-Kalinski MA, Schriger DL, Friedman L, Votey SR. Identification of risk factors for exertional heat-
related illnesses in long-distance cyclists: experience from the California AIDS Ride. Wilderness Environ Med.
2001 Summer;12(2):81-5.
58
Armstrong LE, Epstein Y. Fluid-electrolyte balance during labor and exercise: concepts and misconceptions. Int J
Sport Nutr. 1999 Mar;9(1):1-12.
59
McLellan TM. Sex-related differences in thermoregulatory responses while wearing protective clothing. Eur J
Appl Physiol Occup Physiol 1998 Jun;78(1):28-37.
60
Paolone AM, Wells CL, Kelly GT. Sexual variations in thermoregulation during heat stress. Aviat Space Environ
Med. 1978 May;49(5):715-9.
61
Carter R 3rd, Cheuvront SN, Williams JO, Kolka MA, Stephenson LA, Sawka MN, Amoroso PJ. Epidemiology
of hospitalizations and deaths from heat illness in soldiers. Med Sci Sports Exerc. 2005 Aug;37(8):1338-44.
62
Nunneley SA. Physiological responses of women to thermal stress: a review. Med Sci Sports. 1978
Winter;10(4):250-5.
63
Horvath SM, Drinkwater BL. Thermoregulation and the menstrual cycle. Aviat Space Environ Med. 1982
Aug;53(8):790-4.
64
Tenaglia SA, McLellan TM, Klentrou PP. Influence of menstrual cycle and oral contraceptives on tolerance to
uncompensable heat stress. Eur J Appl Physiol Occup Physiol. 1999 Jul;80(2):76-83.
65
Kenney WL. A review of comparative responses of men and women to heat stress. Environ Res. 1985
Jun;37(1):1-11.
66
Layde PM, Edmonds LD, Erickson JD. Maternal fever and neural tube defects.
Teratology. 1980 Feb;21(1):105-8.
67
Hu H, Besser M. Atmospheric variations, noise, and vibration. In Paul M, ed. Occupational and environmental
reproductive hazards: a guide for clinicians. Baltimore: Williams & Wilkins, 1993:218-232.
68
Anderson SJ, Griesemer BA, Johnson MD, Martin TJ, McLain LG, Rowland TW, Small E. Climatic heat stress
and the exercising child and adolescent. American Academy of Pediatrics. Committee on Sports Medicine and
Fitness. Pediatrics. 2000 Jul;106(1 Pt 1):158-9.
69
Kenney WL, Hodgson JL. Heat tolerance, thermoregulation and ageing. Sports Med. 1987 Nov-Dec;4(6):446-56.
70
Yousef MK, Sagawa S, Shiraki K. Thermoregulatory responses of the elderly population. J UOEH. 1986 Jun
1;8(2):219-27.
71
Kenney WL, Hodgson JL. Heat tolerance, thermoregulation and ageing. Sports Med. 1987 Nov-Dec;4(6):446-56.
72
Miescher E, Fortney SM. Responses to dehydration and rehydration during heat exposure in young and older men.
Am J Physiol. 1989 Nov;257(5 Pt 2):R1050-6.
73
Tanaka M. Local skin thermal responses to heat radiation. Sangyo Igaku. 1985 Mar;27(2):90-6.
74
Yousef MK, Dill DB, Vitez TS, Hillyard SD, Goldman AS. Thermoregulatory responses to desert heat: age, race
and sex. J Gerontol. 1984 Jul;39(4):406-14.
75
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
76
Sawka MN, Latzka WA, Montain SJ, Cadarette BS, Kolka MA, Kraning KK 2nd, Gonzalez RR. Physiologic
tolerance to uncompensable heat: intermittent exercise, field vs laboratory. Med Sci Sports Exerc. 2001
Mar;33(3):422-30.
77
Takamata A, Yoshida T, Nishida N, Morimoto T. Relationship of osmotic inhibition in thermoregulatory
responses and sweat sodium concentration in humans. Am J Physiol Regul Integr Comp Physiol. 2001
Mar;280(3):R623-9.
78
Nielsen B. Heat acclimation--mechanisms of adaptation to exercise in the heat. Int J Sports Med. 1998 Jun;19
Suppl 2:S154-6.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
90
79
Shapiro Y, Moran D, Epstein Y. Acclimatization strategies--preparing for exercise in the heat. Int J Sports Med.
1998 Jun;19 Suppl 2:S161-3.
80
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. 1991
Nov;12(5):302-12.
81
Radakovic SS, Maric J, Surbatovic M, Radjen S, Stefanova E, Stankovic N, Filipovic N. Effects of acclimation on
cognitive performance in soldiers during exertional heat stress. Mil Med. 2007 Feb;172(2):133-6.
82
Francesconi R, Maher J, Bynum G, Mason J. Recurrent heat exposure: effects on levels of plasma and urinary
sodium and potassium in resting and exercising men. Aviat Space Environ Med. 1977 May;48(5):399-404.
83
Francesconi R, Maher J, Bynum G, Mason J. Recurrent heat exposure: effects on levels of plasma and urinary
sodium and potassium in resting and exercising men. Aviat Space Environ Med. 1977 May;48(5):399-404.
84
Febbraio MA, Snow RJ, Hargreaves M, Stathis CG, Martin IK, Carey MF. Muscle metabolism during exercise
and heat stress in trained men: effect of acclimation. J Appl Physiol. 1994 Feb;76(2):589-97.
85
Neufer PD, Young AJ, Sawka MN. Gastric emptying during exercise: effects of heat stress and hypohydration.
Eur J Appl Physiol Occup Physiol. 1989;58(4):433-9.
86
Garden JW, Wilson ID, Rasch PJ. Optimal time of exposure required to produce acclimatization to a hot-wet
environment. Vol. XV, No. 22. MF022.03.04-8002.3. Res Rep U S Nav Med Field Res Lab. 1965 Aug;:1-24.
87
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. 1991
Nov;12(5):302-12.
88
Epstein Y, Moran DS, Shapiro Y, Sohar E, Shemer J. Exertional heat stroke: a case series. Med Sci Sports Exerc.
1999 Feb;31(2):224-8.
89
Gill N, Sleivert G. Effect of daily versus intermittent exposure on heat acclimation. Aviat Space Environ Med.
2001 Apr;72(4):385-90.
90
Gill N, Sleivert G. Effect of daily versus intermittent exposure on heat acclimation. Aviat Space Environ Med.
2001 Apr;72(4):385-90.
91
Gisolfi CV, Cohen JS. Relationships among training, heat acclimation, and heat tolerance in men and women: the
controversy revisited. Med Sci Sports. 1979 Spring;11(1):56-9.
92
Shapiro Y, Moran D, Epstein Y. Acclimatization strategies--preparing for exercise in the heat. Int J Sports Med.
1998 Jun;19 Suppl 2:S161-3.
93
Garden JW, Wilson ID, Rasch PJ. Optimal time of exposure required to produce acclimatization to a hot-wet
environment. Vol. XV, No. 22. MF022.03.04-8002.3. Res Rep U S Nav Med Field Res Lab. 1965 Aug;:1-24.
94
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med. 1991
Nov;12(5):302-12.
95
Curley MD, Hawkins RN. Cognitive performance during a heat acclimatization regimen. Aviat Space Environ
Med. 1983 Aug;54(8):709-13.
96
Aoyagi Y, McLellan TM, Shephard RJ. Effects of 6 versus 12 days of heat acclimation on heat tolerance in lightly
exercising men wearing protective clothing. Eur J Appl Physiol Occup Physiol. 1995;71(2-3):187-96.
97
Aoyagi Y, McLellan TM, Shephard RJ. Effects of 6 versus 12 days of heat acclimation on heat tolerance in lightly
exercising men wearing protective clothing. Eur J Appl Physiol Occup Physiol. 1995;71(2-3):187-96.
98
Aoyagi Y, McLellan TM, Shephard RJ. Effects of endurance training and heat acclimation on psychological strain
in exercising men wearing protective clothing. Ergonomics. 1998 Mar;41(3):328-57.
99
Aoyagi Y, McLellan TM, Shephard RJ. Effects of training and acclimation on heat tolerance in exercising men
wearing protective clothing. Eur J Appl Physiol Occup Physiol. 1994;68(3):234-45.
100
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
101
Horstman DH, Christensen E. Acclimatization to dry heat: active men vs. active women. J Appl Physiol. 1982
Apr;52(4):825-31.
102
Buskirk ER, Iampietro PF, Bass DE. Work performance after dehydration: effects of physical conditioning and
heat acclimatization. 1958. Wilderness Environ Med. 2000 Fall;11(3):204-8.
103
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
104
Pichan G, Sridharan K, Swamy YV, Joseph S, Gautam RK. Physiological acclimatization to heat after a spell of
cold conditioning in tropical subjects. Aviat Space Environ Med. 1985 May;56(5):436-40.
105
Pivarnik JM, Senay LC Jr. Effects of exercise detraining and deacclimation to the heat on plasma volume
dynamics. Eur J Appl Physiol Occup Physiol. 1986;55(2):222-8.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
91
106
Kaufman FL, Mills DE, Hughson RL, Peake GT. Effects of bromocriptine on sweat gland function during heat
acclimatization. Horm Res. 1988;29(1):31-8.
107
Sawka MN, Montain SJ, Latzka WA. Hydration effects on thermoregulation and performance in the heat.
Comp Biochem Physiol A Mol Integr Physiol. 2001 Apr;128(4):679-90.
108
Freund BJ, Sawka MN. Technical note no. T95-4 human fluid balance and dehydration during cold weather
military operations. U.S. Army Research Institute of Environmental Medicine, Natick, MA. December 1994.
109
Grucza R, Lecroart JL, Carette G, Hauser JJ, Houdas Y. Effect of voluntary dehydration on thermoregulatory
responses to heat in men and women. Eur J Appl Physiol Occup Physiol. 1987;56(3):317-22.
110
Gardner JW. Death by water intoxication. Mil Med. 2002 May;167(5):432-4.
111
Garigan TP, Ristedt DE. Death from hyponatremia as a result of acute water intoxication in an Army basic
trainee. Mil Med. 1999 Mar;164(3):234-8.
112
Sawka MN, Latzka WA, Matott RP, Montain SJ. Hydration effects on temperature regulation. Int J Sports Med.
1998 Jun;19 Suppl 2:S108-10.
113
Maxwell NS, Gardner F, Nimmo MA. Intermittent running: muscle metabolism in the heat and effect of
hypohydration. Med Sci Sports Exerc. 1999 May;31(5):675-83.
114
Murray R. Rehydration strategies--balancing substrate, fluid, and electrolyte provision. Int J Sports Med. 1998
Jun;19 Suppl 2:S133-5.
115
Cheung SS, McLellan TM. Heat acclimation, aerobic fitness, and hydration effects on tolerance during
uncompensable heat stress. J Appl Physiol. 1998 May;84(5):1731-9.
116
Kenney WL, Tankersley CG, Newswanger DL, Hyde DE, Puhl SM, Turner NL. Age and hypohydration
independently influence the peripheral vascular response to heat stress. J Appl Physiol. 1990 May;68(5):1902-8.
117
Gonzalez-Alonso J, Mora-Rodriguez R, Coyle EF. Stroke volume during exercise: interaction of environment
and hydration. Am J Physiol Heart Circ Physiol. 2000 Feb;278(2):H321-30.
118
Rehrer NJ. Fluid and electrolyte balance in ultra-endurance sport. Sports Med. 2001;31(10):701-15.
119
Rehrer NJ. Fluid and electrolyte balance in ultra-endurance sport. Sports Med. 2001;31(10):701-15.
120
Neufer PD, Young AJ, Sawka MN. Gastric emptying during exercise: effects of heat stress and hypohydration.
Eur J Appl Physiol Occup Physiol. 1989;58(4):433-9.
121
Sawka MN, Montain SJ, Latzka WA. Hydration effects on thermoregulation and performance in the heat.
Comp Biochem Physiol A Mol Integr Physiol. 2001 Apr;128(4):679-90.
122
Rehrer NJ. Fluid and electrolyte balance in ultra-endurance sport. Sports Med. 2001;31(10):701-15.
123
Cohen BS, Nelson AG, Prevost MC, Thompson GD, Marx BD, Morris GS. Effects of caffeine ingestion on
endurance racing in heat and humidity. Eur J Appl Physiol Occup Physiol. 1996;73(3-4):358-63.
124
Savdie E, Prevedoros H, Irish A, Vickers C, Concannon A, Darveniza P, Sutton JR. Heat stroke following Rugby
League football. Med J Aust. 1991 Nov 4;155(9):636-9.
125
Franklin QJ. Sudden death after typhoid and Japanese encephalitis vaccination in a young male taking
pseudoephedrine. Mil Med. 1999 Feb;164(2):157-9.
126
Bailes JE, Cantu RC, Day AL. The neurosurgeon in sport: awareness of the risks of heatstroke and dietary
supplements. Neurosurgery. 2002 Aug;51(2):283-6; discussion 286-8.
127
Crandall CG, Vongpatanasin W, Victor RG. Mechanism of cocaine-induced hyperthermia in humans. Ann Intern
Med. 2002 Jun 4;136(11):785-91.
128
Navy Environmental Health Center. Unpublished report.
129
Kaufman FL, Mills DE, Hughson RL, Peake GT. Effects of bromocriptine on sweat gland function during heat
acclimatization. Horm Res. 1988;29(1):31-8.
130
Gordon NF, Duncan JJ. Effect of beta-blockers on exercise physiology: implications for exercise training. Med
Sci Sports Exerc. 1991 Jun;23(6):668-76.
131
Freund BJ, Joyner MJ, Jilka SM, Kalis J, Nittolo JM, Taylor JA, Peters H, Feese G, Wilmore JH.
Thermoregulation during prolonged exercise in heat: alterations with beta-adrenergic blockade. J Appl Physiol. 1987
Sep;63(3):930-6.
132
PDR.net. Lithium carbonate tablets USP (Roxane). Copyright © 2002 by Medical Economics Company, Inc. at
Montvale, NJ 07645. All rights reserved.
http://physician.pdr.net/HomePage_template.jsp
133
Eustatia-Rutten CF, Tamsma JT, Meinders AE. Lithium-induced nephrogenic diabetes insipidus.
Neth J Med. 2001 Mar;58(3):137-42.
134
Wagenmakers AJ, Brookes JH, Coakley JH, Reilly T, Edwards RH. Exercise-induced activation of the branched-
chain 2-oxo acid dehydrogenase in human muscle. Eur J Appl Physiol Occup Physiol. 1989;59(3):159-67.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
92
135
Smith IK. Death by 100 degrees Korey Stringer's tragic end reminds us that heatstroke can hit with surprising
speed. How to protect yourself. Time Mag. August 13, 2001.
136
Montain SJ, Latzka WA, Sawka MN. Fluid replacement recommendations for training in hot weather.
Mil Med. 1999 Jul;164(7):502-8.
137
Montain SJ, Latzka WA, Sawka MN. Fluid replacement recommendations for training in hot weather. Mil Med.
1999 Jul;164(7):502-8.
138
NAVOSH. Navy occupational safety and health (NAVOSH) program manual for forces afloat OPNAV
instruction 5100.19D CH-1 volume 1 NAVOSH and major hazard-specific programs. Department of the Navy,
Office of the Chief of Naval Operations. 30 August 2001.
139
Sawka MN, Latzka WA, Montain SJ, Cadarette BS, Kolka MA, Kraning KK 2nd, Gonzalez RR. Physiologic
tolerance to uncompensable heat: intermittent exercise, field vs laboratory. Med Sci Sports Exerc 2001
Mar;33(3):422-30.
140
Williams MJ. Marine Corps Order 6200.1E. Enclosure 4 Heat Condition Flag Warning System. Department of
The Navy. Headquarters United States Marine Corps. 2 Navy Annex, Washington, DC 20380-1775. 6 Jun 2002.
http://www.oki.med.navy.mil/PopHealth/DOCUMENT/MCO%206200.1E.pdf
141
ACGIH Worldwide. 2005 TLVs and BEIs Based on the Documentation of the Threshold Limit Values for
Chemical Substances and Physical Agents & Biological Exposure Indices. American Conference of Governmental
Industrial Hygienists, Cincinnati. 2005:179.
142
Maxwell NS, Gardner F, Nimmo MA. Intermittent running: muscle metabolism in the heat and effect of
hypohydration. Med Sci Sports Exerc. 1999 May;31(5):675-83.
143
Sawka MN, Young AJ, Cadarette BS, Levine L, Pandolf KB. Influence of heat stress and acclimation on
maximal aerobic power. Eur J Appl Physiol Occup Physiol. 1985;53(4):294-8.
144
Febbraio MA, Snow RJ, Hargreaves M, Stathis CG, Martin IK, Carey MF. Muscle metabolism during exercise
and heat stress in trained men: effect of acclimation. J Appl Physiol. 1994 Feb;76(2):589-97.
145
Sawka MN, Young AJ, Cadarette BS, Levine L, Pandolf KB. Influence of heat stress and acclimation on
maximal aerobic power. Eur J Appl Physiol Occup Physiol. 1985;53(4):294-8.
146
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
147
Koller M, Stidl HG, Kundi M, Haider M. Effect of various furniture covering fabrics on heat regulation and
comfort [German]. Zentralbl Bakteriol Mikrobiol Hyg [B]. 1982 Aug;176(4):291-304.
148
Gavin TP, Babington JP, Harms CA, Ardelt ME, Tanner DA, Stager JM. Clothing fabric does not affect
thermoregulation during exercise in moderate heat. Med Sci Sports Exerc. 2001 Dec;33(12):2124-30.
149
McLaren C, Null J, Quinn J. Heat stress from enclosed vehicles: moderate ambient temperatures cause significant
temperature rise in enclosed vehicles. Pediatrics. 2005 Jul;116(1):e109-12.
150
Zhou Y, Li L, Liu L, Jia D, Zhang X, Fowler DR, Xu X. Heat stroke deaths caused by electric blankets: case
report and review of the literature. Am J Forensic Med Pathol. 2006 Dec;27(4):324-7.
151
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
152
Moseley PL. Heat shock proteins and heat adaptation of the whole organism. J Appl Physiol. 1997
Nov;83(5):1413-7.
153
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
154
Jentjens RL, Wagenmakers AJ, Jeukendrup AE. Heat stress increases muscle glycogen use but reduces the
oxidation of ingested carbohydrates during exercise. J Appl Physiol. 2002 Apr;92(4):1562-72.
155
Febbraio MA. Alterations in energy metabolism during exercise and heat stress. Sports Med. 2001;31(1):47-59.
156
Wagner GS, Scarbossa EB. 59 Electrocardiography. In Topol EJ, Califf RM. Textbook of cardiovascular
medicine. © 2002 by Lippincott Williams & Wilkins, Philadelphia.
157
Paolone AM, Lanigan WT, Lewis RR, Goldstein MJ. Effects of a postexercise sauna bath on ECG pattern and
other physiologic variables. Aviat Space Environ Med. 1980 Mar;51(3):224-9.
158
HEW. Occupational exposures to hot environments. US Department of Health, Education and Welfare. HSM 72-
10269;1982:188.
159
Wilson TE, Cui J, Zhang R, Crandall CG. Heat stress reduces cerebral blood velocity and markedly impairs
orthostatic tolerance in humans. Am J Physiol Regul Integr Comp Physiol. 2006 Nov;291(5):R1443-8. Epub 2006
Jun 8.
160
Carter R 3rd, Cheuvront SN, Vernieuw CR, Sawka MN. Hypohydration and prior heat stress exacerbates
decreases in cerebral blood flow velocity during standing. J Appl Physiol. 2006 Dec;101(6):1744-50. Epub 2006
Aug 17.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
93
161
Clanton TL, Zuo L, Klawitter P. Oxidants and skeletal muscle function: physiologic and pathophysiologic
implications. Proc Soc Exp Biol Med. 1999 Dec;222(3):253-62.
162
CHIPPM. TB MED 507/AFPAM 48-52(I) Department of the Army technical bulletin heat stress control and heat
casualty management. Headquarters, Departments of the Army and Air Force. Washington, DC. 7 March 2003.
163
CDC. Heat-related illnesses and deaths -- Missouri, 1998, and United States, 1979—1996. Centers for Disease
Control and Prevention. Morbidity and Mortality Weekly Report. MMWR Weekly June 11, 1999 48(22);469-472.
164
Jones BH, chair, DoD Injury Surveillance and Prevention Work Group. Atlas of injuries in the U.S. armed forces.
A report by the Department of Defense Injury Surveillance and Prevention Work Group for the Assistant Deputy
Under Secretary of Defense for Safety and Occupational Health. Supplement to Military Medicine, International
Journal of AMSUS, vol 164, no 8. DoD Injury Surveillance and Prevention Work Group. August 1999.
165
Dickinson JG. Heat illness in the services. J R Army Med Corps. 1994 Feb;140(1):7-12.
166
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
167
Jokinen E, Valimaki I, Antila K, Seppanen A, Tuominen J. Children in sauna: cardiovascular adjustment.
Pediatrics. 1990 Aug;86(2):282-8.
168
Tayeb OS, Marzouki ZM. Tympanic thermometry in heat stroke: is it justifiable? Clin Physiol Biochem.
1989;7(5):255-62.
169
Dromer C, Leba Q, Guenard H. Determinants of the difference between expired and core temperatures: effect of
a breath-hold. Pflugers Arch. 2000 Sep;440(5):778-83.
170
Newman BH, Martin CA. The effect of hot beverages, cold beverages, and chewing gum on oral temperature.
Transfusion. 2001 Oct;41(10):1241-3.
171
Newman BH, Martin CA. The effect of hot beverages, cold beverages, and chewing gum on oral temperature.
Transfusion. 2001 Oct;41(10):1241-3.
172
Sugarek NJ. Temperature lowering after iced water. Enhanced effects in the elderly. J Am Geriatr Soc. 1986
Jul;34(7):526-9.
173
Thomas KA, Savage MV, Brengelmann GL. Effect of facial cooling on tympanic temperature. Am J Crit Care.
1997 Jan;6(1):46-51.
174
Shibasaki M, Kondo N, Tominaga H, Aoki K, Hasegawa E, Idota Y, Moriwaki T. Continuous measurement of
tympanic temperature with a new infrared method using an optical fiber. J Appl Physiol. 1998 Sep;85(3):921-6.
175
Ash CJ, Cook JR, McMurry TA, Auner CR. The use of rectal temperature to monitor heat stroke. Mo Med. 1992
May;89(5):283-8.
176
Bloch EC, Ginsberg B, Binner RA Jr. The esophageal temperature gradient in anesthetized children. J Clin
Monit. 1993 Apr;9(2):73-7.
177
Livingstone SD, Grayson J, Frim J, Allen CL, Limmer RE. Effect of cold exposure on various sites of core
temperature measurements. J Appl Physiol. 1983 Apr;54(4):1025-31.
178
De Jong UW, Day NE, Mounier-Kuhn PL, Haguenauer JP. The relationship between the ingestion of hot coffee
and intraoesophageal temperature. Gut. 1972 Jan;13(1):24-30.
179
Brauer A, Weyland W, Fritz U, Schuhmann MU, Schmidt JH, Braun U. Determination of core body temperature.
A comparison of esophageal, bladder, and rectal temperature during postoperative rewarming [German].
Anaesthesist. 1997 Aug;46(8):683-8.
180
Dickinson JG. Heat illness in the services. J R Army Med Corps. 1994 Feb;140(1):7-12.
181
Sulman FG. Migraine and headache due to weather and allied causes and its specific treatment.
Ups J Med Sci Suppl. 1980;31:41-4.
182
Sulman FG, Tal E, Pfeifer Y, Superstine. Intermittent hyperthyreosis -- a heat stress syndrome.
Horm Metab Res. 1975 Sep;7(5):424-8.
183
Sulman FG. Migraine and headache due to weather and allied causes and its specific treatment.
Ups J Med Sci Suppl. 1980;31:41-4.
184
Steadman’s medical dictionary version 1.5 based on Steadman’s medical dictionary, 25
th
edition. William &
Wilkins. 1994. Software copyright 1993 WordPerfect Corporation.
185
Donoghue AM, Sinclair MJ. Miliaria rubra of the lower limbs in underground miners. Occup Med (Lond). 2000
Aug;50(6):430-3.
186
Noojin RO. Dermatology a practitioner’s guide. Medical Examination Publishing Company, Inc. New York.
1977.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
94
187
Merck. Miliaria (prickly heat). In Beers MH, Berkow R, eds. The Merck Manual of Diagnosis and Therapy
Seventeenth Edition Centennial Edition. Section 10 dermatologic disorders. Chapter 124 disorders of sweating.
Merck & Co., Inc. Whitehouse Station. 1999.
188
Noojin RO. Dermatology a practitioner’s guide. Medical Examination Publishing Company, Inc. New York.
1977.
189
Pandolf KB, Griffin TB, Munro EH, Goldman RF. Heat intolerance as a function of percent of body surface
involved with miliaria rubra. Am J Physiol. 1980 Sep;239(3):R233-40.
190
Helm TN, Spigel GT, Helm KF. Erythema ab igne caused by a car heater. Cutis. 1997 Feb;59(2):81-2.
191
Helm TN, Spigel GT, Helm KF. Erythema ab igne caused by a car heater. Cutis. 1997 Feb;59(2):81-2.
192
de Jong EM, Koopman RJ, van de Kerkhof PC. Erythema ab igne [Dutch]. Ned Tijdschr Geneeskd. 1995 Jan
28;139(4):192-4.
193
Baruchin AM. Erythema ab igne--a neglected entity? Burns. 1994 Oct;20(5):460-2.
194
de Jong EM, Koopman RJ, van de Kerkhof PC. Erythema ab igne [Dutch]. Ned Tijdschr Geneeskd. 1995 Jan
28;139(4):192-4.
195
Olumide YM, Odunowo BD, Odiase AO. Regional dermatoses in the African. Part I. Facial hypermelanosis. Int J
Dermatol. 1991 Mar;30(3):186-9.
196
Yasuda K, Wada E, Kitagawa N, Ikeda M, Kodama H. Palmar erythema ab igne without detectable type IV
collagen at the basement membrane zone. J Dermatol. 1996 Jul;23(7):484-8.
197
Ashby M. Erythema ab igne in cancer patients. J R Soc Med. 1985 Nov;78(11):925-7.
198
Akasaka T, Kon S. Two cases of squamous cell carcinoma arising from erythema ab igne [Japanese]. Nippon
Hifuka Gakkai Zasshi. 1989 May;99(6):735-42.
199
Rhind SG, Gannon GA, Shek PN, Brenner IK, Severs Y, Zamecnik J, Buguet A, Natale VM, Shephard RJ,
Radomski MW. Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset
redistribution. J Appl Physiol. 1999 Sep;87(3):1178-85.
200
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
201
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
202
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
203
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
204
Schmidt EW, Nichols CG. Chapter 387 heat- and sun-related illnesses. In Harwood-Nuss A, Wolfson AB,
Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and
pressure- related illness and injury. Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
205
McGee SR. Muscle cramps. Arch Intern Med. 1990 Mar;150(3):511-8.
206
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
207
Bergeron MF. Heat cramps during tennis: a case report. Int J Sport Nutr. 1996 Mar;6(1):62-8.
208
Bergeron MF. Heat cramps during tennis: a case report. Int J Sport Nutr. 1996 Mar;6(1):62-8.
209
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
210
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
211211
CDC. Heat-related illnesses and deaths -- Missouri, 1998, and United States, 1979—1996. Centers for Disease
Control and Prevention. Morbidity and Mortality Weekly Report. MMWR Weekly June 11, 1999 48(22);469-472.
212
WHO. International classification of diseases : 9th revision, clinical modification, ICD-9-CM. World Health
Organization Commission on Professional and Hospital Activities. Ann Arbor;1978.
213
Backer HD, Shopes E, Collins SL, Barkan H. Exertional heat illness and hyponatremia in hikers. Am J Emerg
Med. 1999 Oct;17(6):532-9.
214
O'Brien KK, Montain SJ, Corr WP, Sawka MN, Knapik JJ, Craig SC. Hyponatremia associated with
overhydration in U.S. Army trainees. Mil Med. 2001 May;166(5):405-10
215
Backer HD, Shopes E, Collins SL, Barkan H. Exertional heat illness and hyponatremia in hikers. Am J Emerg
Med. 1999 Oct;17(6):532-9.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
95
216
Schmidt EW, Nichols CG. Chapter 387 heat- and sun-related illnesses. In Harwood-Nuss A, Wolfson AB,
Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and
pressure- related illness and injury. Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
217
Noltkamper D. Camp LeJeune Emergency Department. E-mail communication. 16 March 2005.
218
Wexler RK. Evaluation and treatment of heat-related illnesses. Am Fam Physician. 2002 Jun 1;65(11):2307-14.
219
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
220
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
221
Armstrong LE, Maresh CM. The induction and decay of heat acclimatisation in trained athletes. Sports Med.
1991 Nov;12(5):302-12.
222
Wexler RK. Evaluation and treatment of heat-related illnesses. Am Fam Physician. 2002 Jun 1;65(11):2307-14.
223
Nadel E, Cullen MR. Thermal stressors. In Rosenstock L, Cullen MR, eds. Textbook of Clinical Occupational
and Environmental Medicine. W.B. Saunders Company, Philadelphia;1994:658-666.
224
Hansen RD, Olds TS, Richards DA, Richards CR, Leelarthaepin B. Infrared thermometry in the diagnosis and
treatment of heat exhaustion. Int J Sports Med. 1996 Jan;17(1):66-70.
225
Londer M, Hammer D, Kelen GD. Chap 27 Fluid and Electrolyte Problems, in Tintinalli JE, Kelen GD,
Stapczynski JS, eds. Emergency Medicine: A Comprehensive Study Guide 6th edition. McGraw-Hill
Professional;October 14, 2003:Pages 1183-90.
226
Robbins AS. Hypothermia and heat stroke: protecting the elderly patient. Geriatrics. 1989 Jan;44(1):73-7, 80.
227
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
228
Ikeda Y, Sakemi T, Nishihara G, Nakamura M, Fujisaki T, Koh T, Tomiyoshi Y, Emura S, Taki K. Efficacy of
blood purification therapy for heat stroke presenting rapid progress of multiple organ dysfunction syndrome: a
comparison of five cases. Intensive Care Med. 1999 Mar;25(3):315-8.
229
CDC. Heat-related illnesses and deaths -- Missouri, 1998, and United States, 1979—1996. Centers for Disease
Control and Prevention. Morbidity and Mortality Weekly Report. MMWR Weekly June 11, 1999 48(22);469-472.
230
Simon, HB. XXIV Hyperthermia, fever, and fever of undetermined origin. 7 Infectious diseases. SAM-CD
Connected®. Dale DC, Federman DD, Eds. WebMD Corporation, New York, October 1999.
231
Shanks NJ, Papworth G. Environmental factors and heatstroke. Occup Med (Lond). 2001 Feb;51(1):45-9.
232
Forester D. Fatal drug-induced heat stroke. JACEP. 1978 Jun;7(6):243-4.
233
Dixit SN, Bushara KO, Brooks BR. Epidemic heat stroke in a midwest community: risk factors, neurological
complications and sequelae. Wis Med J. 1997 May;96(5):39-41.
234
Waters TA. Heat illness: tips for recognition and treatment. Cleve Clin J Med. 2001 Aug;68(8):685-7.
235
Dixit SN, Bushara KO, Brooks BR. Epidemic heat stroke in a midwest community: risk factors, neurological
complications and sequelae. Wis Med J. 1997 May;96(5):39-41.
236
CDC. Heat-related illnesses and deaths -- Missouri, 1998, and United States, 1979—1996. Centers for Disease
Control and Prevention. Morbidity and Mortality Weekly Report. MMWR Weekly June 11, 1999 48(22);469-472.
237
King J, Barnett PS, Kew MC. Drug-induced hyperpyrexia. A case report. S Afr Med J. 1979 Aug 4;56(5):190-1.
238
Lefkowitz D, Ford CS, Rich C, Biller J, McHenry LC Jr. Cerebellar syndrome following neuroleptic induced heat
stroke. J Neurol Neurosurg Psychiatry. 1983 Feb;46(2):183-5.
239
Lew HL, Lee EH, Date ES, Melnik I. Rehabilitation of a patient with heat stroke: a case report. Am J Phys Med
Rehabil. 2002 Aug;81(8):629-32.
240
Simon, HB. XXIV Hyperthermia, fever, and fever of undetermined origin. 7 Infectious diseases. SAM-CD
Connected®. Dale DC, Federman DD, Eds. WebMD Corporation, New York, October 1999.
241
Yu FC, Lu KC, Lin SH, Chen GS, Chu P, Gao GW, Lin YF. Energy metabolism in exertional heat stroke with
acute renal failure. Nephrol Dial Transplant. 1997 Oct;12(10):2087-92.
242
Barthel HJ. Exertion-induced heat stroke in a military setting. Mil Med. 1990 Mar;155(3):116-9.
243
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
244
Simon, HB. XXIV Hyperthermia, fever, and fever of undetermined origin. 7 Infectious diseases. SAM-CD
Connected®. Dale DC, Federman DD, Eds. WebMD Corporation, New York, October 1999.
245
Kerle KK, Nishimura KD. Exertional collapse and sudden death associated with sickle cell trait.
Mil Med. 1996 Dec;161(12):766-7.
246
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
96
247
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
248
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
249
Tham MK, Cheng J, Fock KM. Heat stroke: a clinical review of 27 cases. Singapore Med J. 1989 Apr;30(2):137-
40.
250
Bouchama A, De Vol EB. Acid-base alterations in heatstroke. Intensive Care Med. 2001 Apr;27(4):680-685.
251
Jimenez-Mejias ME, Montano Diaz M, Villalonga J, Bollain Tienda E, Lopez Pardo F, Pineda JA, Gonzalez de la
Puente MA. Classical heatstroke in Spain. Analysis of a series 78 cases [Spanish]. Med Clin (Barc). 1990 Apr
7;94(13):481-6.
252
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
253
Shahid MS, Hatle L, Mansour H, Mimish L. Echocardiographic and Doppler study of patients with heatstroke
and heat exhaustion. Int J Card Imaging. 1999 Aug;15(4):279-85.
254
Shahid MS, Hatle L, Mansour H, Mimish L. Echocardiographic and Doppler study of patients with heatstroke
and heat exhaustion. Int J Card Imaging. 1999 Aug;15(4):279-85.
255
Akhtar MJ, al-Nozha M, al-Harthi S, Nouh MS. Electrocardiographic abnormalities in patients with heat stroke.
Chest. 1993 Aug;104(2):411-4.
256
al-Harthi SS, Nouh MS, al-Arfaj H, Qaraquish A, Akhter J, Nouh RM. Non-invasive evaluation of cardiac
abnormalities in heat stroke pilgrims. Int J Cardiol. 1992 Nov;37(2):151-4.
257
Dunker M, Rehm M, Briegel J, Thiel M, Schelling G. Exertion-related heat stroke. Lethal multiorgan failure
from accidental hyperthermia in a 23 year old athlete [German]. Anaesthesist. 2001 Jul;50(7):500-5.
258
Wakino S, Hori S, Mimura T, Miyatake S, Fujishima S, Aikawa N. A case of severe heat stroke with abnormal
cardiac findings. Int Heart J. 2005 May;46(3):543-50.
259
O'Donnell J, Gleeson AP. Exercise-induced rhabdomyolysis. Eur J Emerg Med. 1998 Sep;5(3):325-6.
260
Moncure M, Brathwaite CE, Samaha E, Marburger R, Ross SE. Carboxyhemoglobin elevation in trauma victims.
J Trauma. 1999 Mar;46(3):424-7.
261
Seto Y, Kataoka M, Tsuge K. Stability of blood carbon monoxide and hemoglobins during heating.
Forensic Sci Int. 2001 Sep 15;121(1-2):144-50.
262
Deleu D, El Siddig A, Kamran S, Kamha AA, Al Omary IY, Zalabany HA. Downbeat nystagmus following
classical heat stroke. Clin Neurol Neurosurg. 2005 Dec;108(1):102-4. Epub 2005 Jan 13.
263
Weigand K, Riediger C, Stremmel W, Flechtenmacher C, Encke J. Are heat stroke and physical exhaustion
underestimated causes of acute hepatic failure? World J Gastroenterol. 2007 Jan 14;13(2):306-9.
264
Shapiro Y, Seidman DS. Field and clinical observations of exertional heat stroke patients. Med Sci Sports Exerc.
1990 Feb;22(1):6-14.
265
Noakes TD. Fluid and electrolyte disturbances in heat illness. Int J Sports Med. 1998 Jun;19 Suppl 2:S146-9.
266
Donoghue ER, Graham MA, Jentzen JM, Lifschultz BD, Luke JL, Mirchandani HG. Criteria for the diagnosis of
heat-related deaths: National Association of Medical Examiners. Position paper. National Association of Medical
Examiners Ad Hoc Committee on the Definition of Heat-Related Fatalities. Am J Forensic Med Pathol. 1997
Mar;18(1):11-4.
267
Ash CJ, Cook JR, McMurry TA, Auner CR. The use of rectal temperature to monitor heat stroke. Mo Med 1992
May;89(5):283-8.
268
Schmidt EW, Nichols CG. Chapter 387 heat- and sun-related illnesses. In Harwood-Nuss A, Wolfson AB,
Linden CH, Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and
pressure- related illness and injury. Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
269
Tham MK, Cheng J, Fock KM. Heat stroke: a clinical review of 27 cases. Singapore Med J. 1989 Apr;30(2):137-
40.
270
Halkin A, Lev D, Szold O, Bidermann P, Bulocnic S, Halpern P, Sorkine P. Severe heat stroke in an intensive
care unit: course of the disease in the intensive care unit, and early and subsequent treatment results [Hebrew].
Harefuah. 1999 Jul;137(1-2):9-13, 88.
271
Vicario SJ, Okabajue R, Haltom T. Rapid cooling in classic heatstroke: effect on mortality rates. Am J Emerg
Med. 1986 Sep;4(5):394-8.
272
Noltkamper D. Camp LeJeune Emergency Department. E-mail communication. 16 March 2005.
273
Waters TA. Heat illness: tips for recognition and treatment. Cleve Clin J Med. 2001 Aug;68(8):685-7.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
97
274
Halkin A, Lev D, Szold O, Bidermann P, Bulocnic S, Halpern P, Sorkine P. Severe heat stroke in an intensive
care unit: course of the disease in the intensive care unit, and early and subsequent treatment results. [Hebrew]
Harefuah. 1999 Jul;137(1-2):9-13, 88.
275
Poulton TJ, Walker RA. Helicopter cooling of heatstroke victims. Aviat Space Environ Med. 1987
Apr;58(4):358-61.
276
Plattner O, Kurz A, Sessler DI, Ikeda T, Christensen R, Marder D, Clough D. Efficacy of intraoperative cooling
methods. Anesthesiology. 1997 Nov;87(5):1089-95.
277
Hadad E, Rav-Acha M, Heled Y, Epstein Y, Moran DS. Heat stroke : a review of cooling methods. Sports Med.
2004;34(8):501-11.
278
Sawka M. E-mail communication with Muller J. 21 March 2005.
279
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
280
Horowitz BZ. The golden hour in heat stroke: use of iced peritoneal lavage. Am J Emerg Med. 1989
Nov;7(6):616-9.
281
Plattner O, Kurz A, Sessler DI, Ikeda T, Christensen R, Marder D, Clough D. Efficacy of intraoperative cooling
methods. Anesthesiology. 1997 Nov;87(5):1089-95.
282
Einer-Jensen N, Baptiste KE, Madsen F, Khorooshi MH. Can intubation harm the brain in critical care situations?
A new simple technique may provide a method for controlling brain temperature. Med Hypotheses. 2002
Mar;58(3):229-31.
283
Wakino S, Hori S, Mimura T, Fujishima S, Hayashi K, Inamoto H, Saruta T, Aikawa N. Heat stroke with
multiple organ failure treated with cold hemodialysis and cold continuous hemodiafiltration: a case report. Ther
Apher Dial. 2005 Oct;9(5):423-8.
284
Bouchama A, Cafege A, Devol EB, Labdi O, el-Assil K, Seraj M. Ineffectiveness of dantrolene sodium in the
treatment of heatstroke. Crit Care Med 1991;19:176-180.
285
Moran D, Epstein Y, Wiener M, Horowitz M. Dantrolene and recovery from heat stroke. Aviat Space Environ
Med. 1999 Oct;70(10):987-9.
286
Chang CK, Chien CH, Chou HL, Lin MT. The protective effect of hypervolemic hemodilution in experimental
heatstroke. Shock. 2001 Aug;16(2):153-8.
287
McNamee T, Forsythe S, Wollmann R, Ndukwu IM. Central pontine myelinolysis in a patient with classic heat
stroke. Arch Neurol. 1997 Aug;54(8):935-6.
288
Pechlaner Ch, Kaneider NC, Djanani A, Sandhofer A, Schratzberger P, Patsch JR. Antithrombin and near-fatal
exertional heat stroke. Acta Med Austriaca. 2002;29(3):107-11.
289
Ikeda Y, Sakemi T, Nishihara G, Nakamura M, Fujisaki T, Koh T, Tomiyoshi Y, Emura S, Taki K. Efficacy of
blood purification therapy for heat stroke presenting rapid progress of multiple organ dysfunction syndrome: a
comparison of five cases. Intensive Care Med. 1999 Mar;25(3):315-8.
290
Anstead GM, Sutton DA, Thompson EH, Weitzman I, Otto RA, Ahuja SK. Disseminated zygomycosis due to
Rhizopus schipperae after heatstroke. J Clin Microbiol. 1999 Aug;37(8):2656-62.
291
Halkin A, Lev D, Szold O, Bidermann P, Bulocnic S, Halpern P, Sorkine P. Severe heat stroke in an intensive
care unit: course of the disease in the intensive care unit, and early and subsequent treatment results. [Hebrew]
Harefuah. 1999 Jul;137(1-2):9-13, 88.
292
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
293
Noltkamper D. Camp LeJeune Emergency Department. E-mail communication. 16 March 2005.
294
Chavoutier-Uzzan F, Bernuau J, Degott C, Rueff B, Benhamou JP. Heatstroke: a rare cause of massive hepatic
necrosis due to hypoxia. [French] Gastroenterol Clin Biol. 1988 Aug-Sep;12(8-9):668-9.
295
Seraj MA, Channa AB, al Harthi SS, Khan FM, Zafrullah A, Samarkandi AH. Are heat stroke patients fluid
depleted? Importance of monitoring central venous pressure as a simple guideline for fluid therapy. Resuscitation.
1991 Feb;21(1):33-9.
296
Seraj MA, Channa AB, al Harthi SS, Khan FM, Zafrullah A, Samarkandi AH. Are heat stroke patients fluid
depleted? Importance of monitoring central venous pressure as a simple guideline for fluid therapy. Resuscitation.
1991 Feb;21(1):33-9.
297
Gisolfi CV, Duchman SM. Guidelines for optimal replacement beverages for different athletic events.
Med Sci Sports Exerc. 1992 Jun;24(6):679-87.
298
Boninsegna A, D'Amelio G, Calzavara M, Bertolini M. Effect of swimming in thermal water on skeletal muscle,
liver and heart glycogen. Clin Physiol Biochem. 1990;8(6):318-21.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
98
299
Sorensen JB, Ranek L. Exertional heatstroke: survival in spite of severe hypoglycemia, liver and kidney damage.
J Sports Med Phys Fitness. 1988 Mar;28(1):108-10.
300
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
301
Seraj MA, Channa AB, al Harthi SS, Khan FM, Zafrullah A, Samarkandi AH. Are heat stroke patients fluid
depleted? Importance of monitoring central venous pressure as a simple guideline for fluid therapy. Resuscitation.
1991 Feb;21(1):33-9.
302
al-Hadramy MS, Ali F. Catecholamines in heat stroke. Mil Med. 1989 May;154(5):263-4.
303
Lin MT. Heatstroke-induced cerebral ischemia and neuronal damage. Involvement of cytokines and monoamines.
Ann N Y Acad Sci. 1997 Mar 15;813:572-80.
304
Ash CJ, Cook JR, McMurry TA, Auner CR. The use of rectal temperature to monitor heat stroke. Mo Med. 1992
May;89(5):283-8.
305
Eichner ER. Treatment of suspected heat illness. Int J Sports Med. 1998 Jun;19 Suppl 2:S150-3.
306
Bouchama A, Knochel JP. Heat stroke. N Engl J Med. 2002 Jun 20;346(25):1978-88.
307
Gader AM, al-Mashhadani SA, al-Harthy SS. Direct activation of platelets by heat is the possible trigger of the
coagulopathy of heat stroke. Br J Haematol. 1990 Jan;74(1):86-92.
308
Francesconi RP, Willis JS, Gaffin SL, Hubbard RW. On the trail of potassium in heat injury. Wilderness Environ
Med. 1997 May;8(2):105-10.
309
Hart GR, Anderson RJ, Crumpler CP, Shulkin A, Reed G, Knochel JP. Epidemic classical heat stroke: clinical
characteristics and course of 28 patients. Medicine (Baltimore). 1982 May;61(3):189-97.
310
Wang AY, Li PK, Lui SF, Lai KN. Renal failure and heatstroke. Ren Fail. 1995 Mar;17(2):171-9.
311
Holt SG, Moore KP. Pathogenesis and treatment of renal dysfunction in rhabdomyolysis.
Intensive Care Med. 2001 May;27(5):803-11.
312
Splendiani G, Mazzarella V, Cipriani S, Pollicita S, Rodio F, Casciani CU. Dialytic treatment of rhabdomyolysis-
induced acute renal failure: our experience. Ren Fail. 2001 Mar;23(2):183-91.
313
Wang AY, Li PK, Lui SF, Lai KN. Renal failure and heatstroke. Ren Fail. 1995 Mar;17(2):171-9.
314
Ross JH, Attwood EC, Atkin GE, Villar RN. A study on the effects of severe repetitive exercise on serum
myoglobin, creatine kinase, transaminases and lactate dehydrogenase. Q J Med. 1983 Spring;52(206):268-79.
315
Wang AY, Li PK, Lui SF, Lai KN. Renal failure and heatstroke. Ren Fail. 1995 Mar;17(2):171-9.
316
Hadad E, Ben-Ari Z, Heled Y, Moran DS, Shani Y, Epstein Y. Liver transplantation in exertional heat stroke: a
medical dilemma. Intensive Care Med. 2004 Jul;30(7):1474-8. Epub 2004 Apr 23.
317
Takahashi K, Chin K, Ogawa K, Kasahara M, Sakaguchi T, Hasegawa S, Sumi K, Nakamura T, Tamaki A,
Mishima M, Nakamura T, Tanaka K. Living donor liver transplantation with noninvasive ventilation for exertional
heat stroke and severe rhabdomyolysis. Liver Transpl. 2005 May;11(5):570-2.
318
Hadad E, Ben-Ari Z, Heled Y, Moran DS, Shani Y, Epstein Y. Liver transplantation in exertional heat stroke: a
medical dilemma. Intensive Care Med. 2004 Jul;30(7):1474-8. Epub 2004 Apr 23.
319
Noltkamper D. Camp LeJeune Emergency Department. E-mail communication. 16 March 2005.
320
Kerle KK, Nishimura KD. Exertional collapse and sudden death associated with sickle cell trait. Am Fam
Physician. 1996 Jul;54(1):237-40.
321
Woodrow G, Brownjohn AM, Turney JH. The clinical and biochemical features of acute renal failure due to
rhabdomyolysis. Ren Fail. 1995 Jul;17(4):467-74.
322
Phinney LT, Gardner JW, Kark JA, Wenger CB. Long-term follow-up after exertional heat illness during recruit
training. Med Sci Sports Exerc. 2001 Sep;33(9):1443-8.
323
Dematte JE, O'Mara K, Buescher J, Whitney CG, Forsythe S, McNamee T, Adiga RB, Ndukwu IM. Near-fatal
heat stroke during the 1995 heat wave in Chicago. Ann Intern Med. 1998 Aug 1;129(3):173-81.
324
Royburt M, Epstein Y, Solomon Z, Shemer J. Long-term psychological and physiological effects of heat stroke.
Physiol Behav. 1993 Aug;54(2):265-7.
325
Albukrek D, Bakon M, Moran DS, Faibel M, Epstein Y. Heat-stroke-induced cerebellar atrophy: clinical course,
CT and MRI findings. Neuroradiology. 1997 Mar;39(3):195-7.
326
Biary N, Madkour MM, Sharif H. Post-heatstroke parkinsonism and cerebellar dysfunction. Clin Neurol
Neurosurg. 1995 Feb;97(1):55-7.
327
Pitt DC, Kriel RL, Wagner NC, Krach LE. Kluver-Bucy syndrome following heat stroke in a 12-year-old girl.
Pediatr Neurol. 1995 Jul;13(1):73-6.
328
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
99
329
Armstrong LE, De Luca JP, Hubbard RW. Time course of recovery and heat acclimation ability of prior
exertional heatstroke patients. Med Sci Sports Exerc. 1990 Feb;22(1):36-48.
330
Epstein Y. Heat intolerance: predisposing factor or residual injury? Med Sci Sports Exerc. 1990 Feb;22(1):29-35.
331
May require log-in and/or registration to access on-line.
332
NAVOSH. OPNAV Instruction 5100.23F Navy Occupational Safety and health (NAVOSH) Program Manual. 15
July 2002.
333
Holland BM, Bates AR, Gray OP, Pearson JF, Wardrop CA. New insulating material in maintenance of body
temperature. Arch Dis Child. 1985 Jan;60(1):47-50.
334
Currier JJ. Chapter 386 hypothermia. In Harwood-Nuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft
PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and pressure- related illness and injury.
Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
335
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
336
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
337
The Eurowinter Group. Cold exposure and winter mortality from ischaemic heart disease, cerebrovascular
disease, respiratory disease, and all causes in warm and cold regions of Europe. The Eurowinter Group.
Lancet. 1997 May 10;349(9062):1341-6.
338
Giesbrecht GG, Hayward JS. Problems and complications with cold-water rescue. Wilderness Environ Med.
2006 Spring;17(1):26-30.
339
Wolberg AS, Meng ZH, Monroe DM 3rd, Hoffman M. A systematic evaluation of the effect of temperature on
coagulation enzyme activity and platelet function. J Trauma. 2004 Jun;56(6):1221-8.
340
Shafi S, Elliott AC, Gentilello L. Is hypothermia simply a marker of shock and injury severity or an independent
risk factor for mortality in trauma patients? Analysis of a large national trauma registry. J Trauma. 2005
Nov;59(5):1081-5.
341
Harris B, Manecke GR Jr, Niemann J, Madani M, Jamieson S. Deep hypothermia and the vascular response to
thiopental. J Cardiothorac Vasc Anesth. 2006 Oct;20(5):678-83. Epub 2006 Jun 22.
342
National Weather Service Forecast Office Chanhassen MN. Press Release: New wind chill temperature index
implemented on November 1st, 2001. United States National Oceanographic and Atmospheric Administration,
National Weather Service Forecast Office Chanhassen MN. November 05, 2001.
http://www.crh.noaa.gov/mpx/windchill_new.html
343
National Weather Service Wilmington Ohio Weather Forecast Office. August, 2001 press release. United States
National Oceanographic and Atmospheric Administration, National Weather Service Wilmington Ohio Weather
Forecast Office.
http://www.erh.noaa.gov/er/iln/tables.htm
344
National Weather Service Wilmington Ohio Weather Forecast Office. August, 2001 press release. United States
National Oceanographic and Atmospheric Administration, National Weather Service Wilmington Ohio Weather
Forecast Office.
http://www.erh.noaa.gov/er/iln/tables.htm
345
National Weather Service Wilmington Ohio Weather Forecast Office. August, 2001 press release. United States
National Oceanographic and Atmospheric Administration, National Weather Service Wilmington Ohio Weather
Forecast Office.
http://www.srh.noaa.gov/FFC/html/metcalc.shtml
346
Murphy R. Meteorological calculator. United States National Oceanographic and Atmospheric Administration,
National Weather Service Peachtree City, GA. September 3, 2001.
347
National Weather Service Wilmington Ohio Weather Forecast Office. August, 2001 press release. United States
National Oceanographic and Atmospheric Administration, National Weather Service Wilmington Ohio Weather
Forecast Office.
http://www.erh.noaa.gov/er/iln/tables.htm
348
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
349
Wittmers LE Jr. Pathophysiology of cold exposure. Minn Med. 2001 Nov;84(11):30-6.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
100
350
York NR, Blundon JA. Effect of water temperature on diving reflex induced bradycardia in humans. Department
of Biology, Rhodes College, Memphis, TN 38112. Unpublished.
http://kesler.biology.rhodes.edu/sciJ/York.html
351
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
352
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
353
Tipton M, Eglin C, Gennser M, Golden F. Immersion deaths and deterioration in swimming performance in cold
water. Lancet. 1999 Aug 21;354(9179):626-9.
354
McArdle WD, Magel JR, Gergley TJ, Spina RJ, Toner MM. Thermal adjustment to cold-water exposure in
resting men and women. J Appl Physiol. 1984 Jun;56(6):1565-71.
355
Nuckton TJ, Claman DM, Goldreich D, Wendt FC, Nuckton JG. Hypothermia and afterdrop following open
water swimming: the Alcatraz/San Francisco Swim Study. Am J Emerg Med. 2000 Oct;18(6):703-7.
356
Young AJ, Sawka MN, Neufer PD, Muza SR, Askew EW, Pandolf KB. Thermoregulation during cold water
immersion is unimpaired by low muscle glycogen levels. J Appl Physiol. 1989 Apr;66(4):1809-16.
357
Shupak A, Weiler-Ravell D, Adir Y, Daskalovic YI, Ramon Y, Kerem D. Pulmonary oedema induced by
strenuous swimming: a field study. Respir Physiol. 2000 Jun;121(1):25-31.
358
Hampson NB, Dunford RG. Pulmonary edema of scuba divers. Undersea Hyperb Med. 1997;24(1):29-33.
359
Gnadinger CA, Colwell CB, Knaut AL. Scuba diving-induced pulmonary edema in a swimming pool.
J Emerg Med. 2001 Nov;21(4):419-21.
360
Shupak A, Weiler-Ravell D, Adir Y, Daskalovic YI, Ramon Y, Kerem D. Pulmonary oedema induced by
strenuous swimming: a field study. Respir Physiol. 2000 Jun;121(1):25-31.
361
Hampson NB, Dunford RG. Pulmonary edema of scuba divers. Undersea Hyperb Med. 1997;24(1):29-33.
362
Cochard G, Arvieux J, Lacour JM, Madouas G, Mongredien H, Arvieux CC. Pulmonary edema in scuba divers:
recurrence and fatal outcome. Undersea Hyperb Med. 2005 Jan-Feb;32(1):39-44.
363
Hoffman RG, Pozos RS. Experimental hypothermia and cold perception. Aviat Space Environ Med. 1989
Oct;60(10 Pt 1):964-9.
364
Keatinge WR, Mason AC, Millard CE, Newstead CG. Effects of fluctuating skin temperature on
thermoregulatory responses in man. J Physiol. 1986 Sep;378:241-52.
365
Park KS, Choi JK, Park YS. Cardiovascular regulation during water immersion. Appl Human Sci. 1999
Nov;18(6):233-41.
366
Hayward JS, Eckerson JD. Physiological responses and survival time prediction for humans in ice-water. Aviat
Space Environ Med. 1984 Mar;55(3):206-11.
367
Hayward JS, Eckerson JD, Collis ML. Thermal balance and survival time prediction of man in cold water. Can J
Physiol Pharmacol. 1975 Feb;53(1):21-32.
368
Hayward JS, Eckerson JD. Physiological responses and survival time prediction for humans in ice-water. Aviat
Space Environ Med. 1984 Mar;55(3):206-11.
369
Steinman AM, Hayward JS, Nemiroff MJ, Kubilis PS. Immersion hypothermia: comparative protection of anti-
exposure garments in calm versus rough seas. Aviat Space Environ Med. 1987 Jun;58(6):550-8.
370
U.S. Navy. U.S. Navy cold weather handbook for surface ships. Chief of Naval Operations Surface Ship
Survivability Office OP-03C2 the Pentagon. United States Government Printing Office, Washington;1988:9-4.
371
Thompson, KE. E-mail communication 23 OCT 2005, attributing source of information to Gordon Giesbrecht,
University of Mannitoba.
372
Steinman AM, Hayward JS, Nemiroff MJ, Kubilis PS. Immersion hypothermia: comparative protection of anti-
exposure garments in calm versus rough seas. Aviat Space Environ Med. 1987 Jun;58(6):550-8.
373
Bandopadhyay P, Selvamurthy W. Respiratory changes due to extreme cold in the Arctic environment. Int J
Biometeorol. 1993 Feb;37(1):32-5.
374
Durmowicz AG, Noordeweir E, Nicholas R, Reeves JT. Inflammatory processes may predispose children to
high-altitude pulmonary edema. J Pediatr. 1997 May;130(5):838-40.
375
Thompson, KE. E-mail communication 23 OCT 2005, attributing source of information to Peter Hackett.
376
Sevre K, Bendz B, Hanko E, Nakstad AR, Hauge A, Kasin JI, Lefrandt JD, Smit AJ, Eide I, Rostrup M. Reduced
autonomic activity during stepwise exposure to high altitude. Acta Physiol Scand. 2001 Dec;173(4):409-17.
377
Harirchi I, Arvin A, Vash JH, Zafarmand V. Frostbite: incidence and predisposing factors in mountaineers. Br J
Sports Med. 2005 Dec;39(12):898-901.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
101
378
Daniels F, Jr. Contact cooling of the hand at -20° F. Technical Report EP-22. Quartermaster Research and
Development Center. US Army Natic, MA.
379
Chen F, Nilsson H, Holmer I. Finger cooling by contact with cold aluminium surfaces--effects of pressure, mass
and whole body thermal balance. Eur J Appl Physiol Occup Physiol. 1994;69(1):55-60.
380
Chen F, Nilsson H, Holmer I. Cooling responses of finger in contact with an aluminum surface. Am Ind Hyg
Assoc J. 1994 Mar;55(3):218-22.
381
Anttonen H, Virokannas H. Assessment of cold stress in outdoor work. Arctic Med Res. 1994 Jan;53(1):40-8.
382
Thompson, KE. E-mail communication 23 OCT 2005, referring to field experience and work among Norwegian
military personnel.
383
Anttonen H, Virokannas H. Assessment of cold stress in outdoor work. Arctic Med Res. 1994 Jan;53(1):40-8.
384
Romlin B, Petruson K, Nilsson K. Moderate superficial hypothermia prolongs bleeding time in humans. Acta
Anaesthesiol Scand. 2007 Feb;51(2):198-201. Epub 2006 Nov 10.
385
Malchaire J, Geng Q, Den Hartog E, Havenith G, Holmer I, Piette A, Powell SL, Rintamaki H, Rissanen S.
Temperature limit values for gripping cold surfaces. Ann Occup Hyg. 2002 Mar;46(2):157-63.
386
Malchaire J, Geng Q, Den Hartog E, Havenith G, Holmer I, Piette A, Powell SL, Rintamaki H, Rissanen S.
Temperature limit values for gripping cold surfaces. Ann Occup Hyg. 2002 Mar;46(2):157-63.
387
Daniels F, Jr. Contact cooling of the hand at -20° F. Technical Report EP-22. Quartermaster Research and
Development Center. US Army Natic, MA.
388
Malchaire J, Geng Q, Den Hartog E, Havenith G, Holmer I, Piette A, Powell SL, Rintamaki H, Rissanen S.
Temperature limit values for gripping cold surfaces. Ann Occup Hyg. 2002 Mar;46(2):157-63.
389
Lockhart JM. Effects of body and hand cooling on complex manual performance. J Appl Psychol. 1966
Feb;50(1):57-9.
390
Clark RE, Cohen A. Manual performance as a function of rate of change in hand skin temperature. J Appl
Physiol. 1960 May;15:496-8.
391
Daniels F, Jr. Contact cooling of the hand at -20° F. Technical Report EP-22. Quartermaster Research and
Development Center. US Army Natic, MA.
392
Daniels F, Jr. Contact cooling of the hand at -20° F. Technical Report EP-22. Quartermaster Research and
Development Center. US Army Natic, MA. Quoting from Buettner K. Physical heat balance in man. Chapter VIII-C
in German Aviation Medicine, World War II. Vol. II. Dept. of the Air Force. U.S. Government Printing Office.
393
Shephard RJ. Some consequences of polar stress: data from a transpolar ski-trek. Arctic Med Res. 1991
Jan;50(1):25-9.
394
Pfannstiel G, Walter. [Relationship between temperatures behavior following short-term exposure of fingers to
heat and cold and various anthropometric index values. Contribution on the problem of temperature regulation in
man. [German]. Anthropol Anz. 1976 Mar;35(2-3):117-26.
395
Pettit SE, Marchand I, Graham T. Gender differences in cardiovascular and catecholamine responses to cold-air
exposure at rest. Can J Appl Physiol. 1999 Apr;24(2):131-47.
396
Murray SJ, Shephard RJ, Greaves S, Allen C, Radomski M. Effects of cold stress and exercise on fat loss in
females. Eur J Appl Physiol Occup Physiol. 1986;55(6):610-8.
397
Nunneley SA. Physiological responses of women to thermal stress: a review. Med Sci Sports. 1978
Winter;10(4):250-5.
398
Falk B. Effects of thermal stress during rest and exercise in the paediatric population. Sports Med. 1998
Apr;25(4):221-40.
399
Degroot DW, Kenney WL. Impaired defense of core temperature in aged humans during mild cold stress. Am J
Physiol Regul Integr Comp Physiol. 2007 Jan;292(1):R103-8. Epub 2006 May 25.
400
Mathew L, Purkayastha SS, Jayashankar A, Sharma RP. Responses of high altitude natives a standard cold test at
sea level. Aviat Space Environ Med. 1979 Apr;50(4):372-5.
401
Bittel J. The different types of general cold adaptation in man. Int J Sports Med. 1992 Oct;13 Suppl 1:S172-6.
402
Purkayastha SS, Selvamurthy W, Ilavazhagan G. Peripheral vascular response to local cold stress of tropical men
during sojourn in the Arctic cold region. Jpn J Physiol. 1992;42(6):877-89.
403
Leonard WR, Sorensen MV, Galloway VA, Spencer GJ, Mosher MJ, Osipova L, Spitsyn VA. Climatic
influences on basal metabolic rates among circumpolar populations. Am J Human Biol. 2002 Sep-Oct;14(5):609-20.
404
Savourey G, Vallerand AL, Bittel JH. General and local cold adaptation after a ski journey in a severe arctic
environment. Eur J Appl Physiol Occup Physiol. 1992;64(2):99-105.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
102
405
Kovtoun LT, Krivoschekov SG. Ten-day cold exposures develop adaptation-compensatory mechanisms of
regulation of heat exchange and breathing. Int J Circumpolar Health. 2001 Apr;60(2):312-7.
406
Waag T, Hesselberg O, Reinertsen RE. Heat production during cold water immersion: the role of shivering and
exercise in the development of hypothermia. Arctic Med Res. 1995;54 Suppl 2:60-4.
407
Wilson E, Waring WS. Severe hypotension and hypothermia caused by acute ethanol toxicity. Emerg Med J.
2007 Feb;24(2):e7.
408
Fox GR, Hayward JS, Hobson GN. Effect of alcohol on thermal balance of man in cold water. Can J Physiol
Pharmacol. 1979 Aug;57(8):860-5.
409
Johnston CE, Bristow GK, Elias DA, Giesbrecht GG.Alcohol lowers the vasoconstriction threshold in humans
without affecting core cooling rate during mild cold exposure. Eur J Appl Physiol Occup Physiol. 1996;74(3):293-5.
410
Hackney AC, Coyne JT, Pozos R, Feith S, Seale J. Validity of urine-blood hydrational measures to assess total
body water changes during mountaineering in the sub-Arctic. Arctic Med Res. 1995 Apr;54(2):69-77.
411
Hackney AC, Coyne JT, Pozos R, Feith S, Seale J. Validity of urine-blood hydrational measures to assess total
body water changes during mountaineering in the sub-Arctic. Arctic Med Res. 1995 Apr;54(2):69-77.
412
Milroy WC. Medical operational problems in cold environment, the role of dehydration, caloric intake, and
clothing. Mil Med. 1987 Aug;152(8):397-8.
413
Milroy WC. Medical operational problems in cold environment, the role of dehydration, caloric intake, and
clothing. Mil Med. 1987 Aug;152(8):397-8.
414
Linker RA, Mohr A, Cepek L, Gold R, Prange H. Core hypothermia in multiple sclerosis: case report with
magnetic resonance imaging localization of a thalamic lesion. Mult Scler. 2006 Feb;12(1):112-5.
415
Hemelsoet DM, De Bleecker JL. Post-traumatic spontaneous recurrent hypothermia: a variant of Shapiro's
syndrome. Eur J Neurol. 2007 Feb;14(2):224-7.
416
Bosacki C, Hausfater P, Koenig M, Serratrice J, Piette AM, Cathebras P. Spontaneous hypothermia: a series of
ten cases, place of Shapiro's syndrome [French]. Rev Med Interne. 2005 Aug;26(8):615-23.
417
Thomas JR, Ahlers ST, House JF, Schrot J. Repeated exposure to moderate cold impairs matching-to-sample
performance. Aviat Space Environ Med. 1989 Nov;60(11):1063-7.
418
Wedin B, Vanggaard L, Hirvonen J. "Paradoxical undressing" in fatal hypothermia. J Forensic Sci. 1979
Jul;24(3):543-53.
419
Kinzinger R, Risse M, Puschel K. Irrational behavior in exposure to cold. Paradoxical undressing in hypothermia.
Arch Kriminol. [German]. 1991 Jan-Feb;187(2):47-56.
420
Sessler DI. Mild perioperative hypothermia. N Engl J Med. 1997 Jun 12;336(24):1730-7.
421
Ozaki H, Nagai Y, Tochihara Y. Physiological responses and manual performance in humans following repeated
exposure to severe cold at night. Eur J Appl Physiol. 2001 Apr;84(4):343-9.
422
Barnes WS, Larson MR. Effects of localized hyper- and hypothermia on maximal isometric grip strength. Am J
Phys Med. 1985 Dec;64(6):305-14.
423
Vanggaard L. Physiological reactions to wet-cold. Aviat Space Environ Med. 1975 Jan;46(1):33-6.
424
Kayser B. Nutrition and high altitude exposure. Int J Sports Med. 1992 Oct;13 Suppl 1:S129-32.
425
Kayser B, Acheson K, Decombaz J, Fern E, Cerretelli P. Protein absorption and energy digestibility at high
altitude. J Appl Physiol. 1992 Dec;73(6):2425-31.
426
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
427
van Marken Lichtenbelt WD, Schrauwen P, van De Kerckhove S, Westerterp-Plantenga MS. Individual variation
in body temperature and energy expenditure in response to mild cold. Am J Physiol Endocrinol Metab. 2002
May;282(5):E1077-83.
428
Glickman-Weiss EL, Nelson AG, Hearon CM. Influence of cold water immersion on heat debt and substrate
utilization in males varying in body composition: a retrospective analysis. Wilderness Environ Med. 1995
Aug;6(3):295-303.
429
Koska J, Ksinantova L, Sebokova E, Kvetnansky R, Klimes I, Chrousos G, Pacak K. Endocrine regulation of
subcutaneous fat metabolism during cold exposure in humans. Ann N Y Acad Sci. 2002 Jun;967:500-5.
430
Vallerand AL, Jacobs I. Influence of cold exposure on plasma triglyceride clearance in humans.
Metabolism. 1990 Nov;39(11):1211-8.
431
Tikuisis P, Eyolfson DA, Xu X, Giesbrecht GG. Shivering endurance and fatigue during cold water immersion in
humans. Eur J Appl Physiol. 2002 May;87(1):50-8.
432
Layden JD, Patterson MJ, Nimmo MA. Effects of reduced ambient temperature on fat utilization during
submaximal exercise. Med Sci Sports Exerc. 2002 May;34(5):774-9.
433
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
103
434
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
435
Koska J, Ksinantova L, Sebokova E, Kvetnansky R, Klimes I, Chrousos G, Pacak K. Endocrine regulation of
subcutaneous fat metabolism during cold exposure in humans. Ann N Y Acad Sci. 2002 Jun;967:500-5.
436
Wade GN, Schneider JE, Li HY. Control of fertility by metabolic cues. Am J Physiol. 1996 Jan;270(1 Pt 1):E1-
19.
437
Wittmers LE Jr. Pathophysiology of cold exposure. Minn Med. 2001 Nov;84(11):30-6.
438
Consolazio CF, Schnakenberg DD. Nutrition and the responses to extreme environments. Fed Proc. 1977
Apr;36(5):1673-8.
439
Sheldahl LM, Buskirk ER, Loomis JL, Hodgson JL, Mendez J. Effects of exercise in cool water on body weight
loss. Int J Obes. 1982;6(1):29-42.
440
Haman F, Peronnet F, Kenny GP, Massicotte D, Lavoie C, Scott C, Weber JM. Effect of cold exposure on fuel
utilization in humans: plasma glucose, muscle glycogen, and lipids. J Appl Physiol. 2002 Jul;93(1):77-84.
441
Vallerand AL, Jacobs I. Rates of energy substrates utilization during human cold exposure. Eur J Appl Physiol
Occup Physiol. 1989;58(8):873-8.
442
Vallerand AL, Zamecnik J, Jones PJ, Jacobs I. Cold stress increases lipolysis, FFA Ra and TG/FFA cycling in
humans. Aviat Space Environ Med. 1999 Jan;70(1):42-50.
443
Lean ME, Murgatroyd PR, Rothnie I, Reid IW, Harvey R. Metabolic and thyroidal responses to mild cold are
abnormal in obese diabetic women. Clin Endocrinol (Oxf). 1988 Jun;28(6):665-73.
444
Sheldahl LM, Buskirk ER, Loomis JL, Hodgson JL, Mendez J. Effects of exercise in cool water on body weight
loss. Int J Obes. 1982;6(1):29-42.
445
Srivastava KK, Kumar R. Human nutrition in cold and high terrestrial altitudes. Int J Biometeorol. 1992
Mar;36(1):10-3.
446
Westerterp-Plantenga MS, Westerterp KR, Rubbens M, Verwegen CR, Richelet JP, Gardette B. Appetite at "high
altitude" [Operation Everest III (Comex-'97)]: a simulated ascent of Mount Everest. J Appl Physiol. 1999
Jul;87(1):391-9.
447
Westerterp-Plantenga MS. Effects of extreme environments on food intake in human subjects. Proc Nutr Soc.
1999 Nov;58(4):791-8.
448
Chotani MA, Flavahan S, Mitra S, Daunt D, Flavahan NA. Silent alpha(2C)-adrenergic receptors enable cold-
induced vasoconstriction in cutaneous arteries. Am J Physiol Heart Circ Physiol. 2000 Apr;278(4):H1075-83.
449
Granberg PO. Human physiology under cold exposure. Arctic Med Res. 1991;50 Suppl 6:23-7.
450
Sessler DI, Moayeri A, Stoen R, Glosten B, Hynson J, McGuire J. Thermoregulatory vasoconstriction decreases
cutaneous heat loss. Anesthesiology. 1990 Oct;73(4):656-60.
451
Ozaki H, Nagai Y, Tochihara Y. Physiological responses and manual performance in humans following repeated
exposure to severe cold at night. Eur J Appl Physiol. 2001 Apr;84(4):343-9.
452
Komulainen S, Tahtinen T, Rintamaki H, Virokannas H, Keinanen-Kiukaanniemi S. Blood pressure responses to
whole-body cold exposure: effect of carvedilol. Eur J Clin Pharmacol 2000 Dec;56(9-10):637-42.
453
Kristal-Boneh E, Harari G, Green MS. Seasonal change in 24-hour blood pressure and heart rate is greater among
smokers than nonsmokers. Hypertension. 1997 Sep;30(3 Pt 1):436-41.
454
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
455
Emmett JD. A review of heart rate and blood pressure responses in the cold in healthy subjects and coronary
artery disease patients. J Cardiopulm Rehabil. 1995 Jan-Feb;15(1):19-24.
456
Wagner JA, Horvath SM. Cardiovascular reactions to cold exposures differ with age and gender. J Appl Physiol.
1985 Jan;58(1):187-92.
457
Wittmers LE Jr. Pathophysiology of cold exposure. Minn Med. 2001 Nov;84(11):30-6.
458
Johansson B. Cold and ischaemic heart disease. Int J Circumpolar Health. 2000 Oct;59(3-4):188-91.
459
Melin B, Savourey G. Sports and extreme conditions. Cardiovascular incidence in long term exertion and
extreme temperatures (heat, cold). [French.] Rev Prat. 2001 Jun 30;51(12 Suppl):S28-30.
460
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
461
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
462
Giesbrecht GG. The respiratory system in a cold environment. Aviat Space Environ Med. 1995 Sep;66(9):890-
902.
463
Doubt TJ. Physiology of exercise in the cold. Sports Med. 1991 Jun;11(6):367-81.
464
Bandopadhyay P, Selvamurthy W. Respiratory changes due to extreme cold in the Arctic environment. Int J
Biometeorol. 1993 Feb;37(1):32-5.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
104
465
Eyolfson DA, Tikuisis P, Xu X, Weseen G, Giesbrecht GG. Measurement and prediction of peak shivering
intensity in humans. Eur J Appl Physiol. 2001 Jan-Feb;84(1-2):100-6.
466
Shephard RJ. Adaptation to exercise in the cold. Sports Med. 1985 Jan-Feb;2(1):59-71.
467
Young AJ, Sawka MN, Neufer PD, Muza SR, Askew EW, Pandolf KB. Thermoregulation during cold water
immersion is unimpaired by low muscle glycogen levels. J Appl Physiol. 1989 Apr;66(4):1809-16.
468
Passias TC, Meneilly GS, Mekjavic IB. Effect of hypoglycemia on thermoregulatory responses. J Appl Physiol.
1996 Mar;80(3):1021-32.
469
Eyolfson DA, Tikuisis P, Xu X, Weseen G, Giesbrecht GG. Measurement and prediction of peak shivering
intensity in humans. Eur J Appl Physiol. 2001 Jan-Feb;84(1-2):100-6.
470
Castellani JW, Young AJ, Degroot DW, Stulz DA, Cadarette BS, Rhind SG, Zamecnik J, Shek PN, Sawka MN.
Thermoregulation during cold exposure after several days of exhaustive exercise. J Appl Physiol. 2001
Mar;90(3):939-46.
471
Young AJ, Castellani JW. Exertion-induced fatigue and thermoregulation in the cold. Comp Biochem Physiol A
Mol Integr Physiol. 2001 Apr;128(4):769-76.
472
Castellani JW, Young AJ, Degroot DW, Stulz DA, Cadarette BS, Rhind SG, Zamecnik J, Shek PN, Sawka MN.
Thermoregulation during cold exposure after several days of exhaustive exercise. J Appl Physiol. 2001
Mar;90(3):939-46.
473
Ozaki H, Nagai Y, Tochihara Y. Physiological responses and manual performance in humans following repeated
exposure to severe cold at night. Eur J Appl Physiol. 2001 Apr;84(4):343-9.
474
Ozaki H, Nagai Y, Tochihara Y. Physiological responses and manual performance in humans following repeated
exposure to severe cold at night. Eur J Appl Physiol. 2001 Apr;84(4):343-9.
475
Bittel JH. Heat debt as an index for cold adaptation in men. J Appl Physiol. 1987 Apr;62(4):1627-34.
476
Bittel JH. Heat debt as an index for cold adaptation in men. J Appl Physiol. 1987 Apr;62(4):1627-34.
477
Bittel JH. Heat debt as an index for cold adaptation in men. J Appl Physiol. 1987 Apr;62(4):1627-34.
478
Bittel JH. Heat debt as an index for cold adaptation in men. J Appl Physiol. 1987 Apr;62(4):1627-34.
479
Budd GM, Brotherhood JR, Thomas DW, Beasley FA, Hendrie AL, Jeffery SE, Lincoln GJ, Solaga AT.
Cardiovascular and metabolic responses to noradrenaline in men acclimatized to cold baths. Eur J Appl Physiol
Occup Physiol. 1993;67(5):450-6.
480
Budd GM, Brotherhood JR, Beasley FA, Hendrie AL, Jeffery SE, Lincoln GJ, Solaga AT. Effects of
acclimatization to cold baths on men's responses to whole-body cooling in air. Eur J Appl Physiol Occup Physiol.
1993;67(5):438-49.
481
LeBlanc J. Mechanisms of adaptation to cold. Int J Sports Med. 1992 Oct;13 Suppl 1:S169-72.
482
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
483
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
484
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
485
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
486
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
487
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
488
Rai RM, Selvamurthy W, Purkayastha SS, Malhotra MS. Effect of altitude acclimatization on thermoregulation
efficiency of man. Aviat Space Environ Med. 1978 May;49(5):707-9.
489
Jansky L, Sramek P, Savlikova J, Ulicny B, Janakova H, Horky K. Change in sympathetic activity,
cardiovascular functions and plasma hormone concentrations due to cold water immersion in men. Eur J Appl
Physiol Occup Physiol. 1996;74(1-2):148-52.
490
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
491
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
492
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
105
493
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
494
Jansky L, Janakova H, Ulicny B, Sramek P, Hosek V, Heller J, Parizkova J. Changes in thermal homeostasis in
humans due to repeated cold water immersions. Pflugers Arch. 1996 Jul;432(3):368-72.
495
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
496
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
497
Muza SR, Young AJ, Sawka MN, Bogart JE, Pandolf KB. Respiratory and cardiovascular responses to cold
stress following repeated cold water immersion. Undersea Biomed Res. 1988 May;15(3):165-78.
498
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
499
Budd GM, Brotherhood JR, Thomas DW, Beasley FA, Hendrie AL, Jeffery SE, Lincoln GJ, Solaga AT.
Cardiovascular and metabolic responses to noradrenaline in men acclimatized to cold baths. Eur J Appl Physiol
Occup Physiol. 1993;67(5):450-6.
500
Young AJ, Muza SR, Sawka MN, Gonzalez RR, Pandolf KB. Human thermoregulatory responses to cold air are
altered by repeated cold water immersion. J Appl Physiol. 1986 May;60(5):1542-8.
501
Young AJ, Muza SR, Sawka MN, Pandolf KB. Human vascular fluid responses to cold stress are not altered by
cold acclimation. Undersea Biomed Res. 1987 May;14(3):215-28.
502
Rai RM, Selvamurthy W, Purkayastha SS, Malhotra MS. Effect of altitude acclimatization on thermoregulation
efficiency of man. Aviat Space Environ Med. 1978 May;49(5):707-9.
503
Leblanc J. Factors affecting cold acclimation and thermogenesis in man. Med Sci Sports Exerc. 1988 Oct;20(5
Suppl):S193-6.
504
Savourey G, Barnavol B, Caravel JP, Feuerstein C, Bittel JH. Hypothermic general cold adaptation induced by
local cold acclimation. Eur J Appl Physiol Occup Physiol. 1996;73(3-4):237-44.
505
Purkayastha SS, Selvamurthy W, Ilavazhagan G. Peripheral vascular response to local cold stress of tropical men
during sojourn in the Arctic cold region. Jpn J Physiol. 1992;42(6):877-89.
506
Leblanc J. Factors affecting cold acclimation and thermogenesis in man. Med Sci Sports Exerc. 1988 Oct;20(5
Suppl):S193-6.
507
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
508
LeBlanc J. Mechanisms of adaptation to cold. Int J Sports Med. 1992 Oct;13 Suppl 1:S169-72.
509
Determining cold-stress in full-term newborns through temperature site comparisons. Sch Inq Nurs Pract. 1991
Summer;5(2):113-23; discussion 125-6.
510
Kuroshima A. Regulation of thermoregulatory thermogenesis. [Japanese]. Hokkaido Igaku Zasshi. 1995
Jan;70(1):1-8.
511
Hayward JS, Eckerson JD, Kemna D. Thermal and cardiovascular changes during three methods of resuscitation
from mild hypothermia. Resuscitation. 1984 Feb;11(1-2):21-33.
512
Moran DS, Castellani JW, O'Brien C, Young AJ, Pandolf KB. Evaluating physiological strain during cold
exposure using a new cold strain index. Am J Physiol. 1999 Aug;277(2 Pt 2):R556-64.
513
Castellani JW, Young AJ, O'Brien C, Stulz DA, Sawka MN, Pandolf KB. Cold strain index applied to exercising
men in cold-wet conditions. Am J Physiol Regul Integr Comp Physiol. 2001 Dec;281(6):R1764-8.
514
Tchoua R, Mahamat Y, Loembe PM. Severe hypothermia in a tropical setting. [French]. Med Trop (Mars).
1998;58(2):158-60.
515
Young AJ, O'Brien C, Sawka MN, Gonzalez RR. Physiological problems associated with wearing NBC
protective clothing during cold weather. Aviat Space Environ Med. 2000 Feb;71(2):184-9.
516
Lehmuskallio E. Cold protecting ointments and frostbite. A questionnaire study of 830 conscripts in Finland.
Acta Derm Venereol. 1999 Jan;79(1):67-70.
517
Pache M, Krauchi K, Cajochen C, Wirz-Justice A, Dubler B, Flammer J, Kaiser HJ. Cold feet and prolonged
sleep-onset latency in vasospastic syndrome. Lancet. 2001 Jul 14;358(9276):125-6.
518
Mekjavic IB, Tipton MJ, Gennser M, Eiken O. Motion sickness potentiates core cooling during immersion in
humans. J Physiol. 2001 Sep 1;535(Pt 2):619-23.
519
Stedman’s medical dictionary version 1.5 based on Stedman’s medical dictionary, 25
th
edition. William &
Wilkins. 1994. Software copyright 1993 WordPerfect Corporation.
520
Amblard P. True and false acrocyanoses. [French]. Rev Prat 1998 Oct 1;48(15):1665-8.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
106
521
Blount BW, Pelletier AL. Rosacea: a common, yet commonly overlooked, condition. Am Fam Physician. 2002
Aug 1;66(3):435-40.
522
Berentsen S, Bo K, Shammas FV, Myking AO, Ulvestad E. Chronic cold agglutinin disease of the "idiopathic"
type is a premalignant or low-grade malignant lymphoproliferative disease. APMIS. 1997 May;105(5):354-62.
523
Berentsen S, Tjonnfjord GE, Brudevold R, Gjertsen BT, Langholm R, Lokkevik E, Sorbo JH, Ulvestad E.
Favourable response to therapy with the anti-CD20 monoclonal antibody rituximab in primary chronic cold
agglutinin disease. Br J Haematol. 2001 Oct;115(1):79-83.
524
Kannagi R, Mitsuoka C. Cold agglutinin disease and paroxysmal cold hemoglobinuria. [Japanese.]
Nippon Rinsho. 1996 Sep;54(9):2519-27.
525
Schrier SL. IV Hemoglobinopathies and hemolytic anemias. 5 Hematology. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York. April 1999.
526
Schrier SL. IV Hemoglobinopathies and hemolytic anemias. 5 Hematology. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York. April 1999.
527
Lauchli S, Widmer L, Lautenschlager S. Cold agglutinin disease--the importance of cutaneous signs.
Dermatology. 2001;202(4):356-8.
528
Aroni K, Aivaliotis M, Tsele E, Charalambopoulos D, Davaris P. An unusual panniculitis appearing in the winter
with good response to tetracycline. J Dermatol. 1998 Oct;25(10):677-81.
529
Baruchin AM, Scharf S. Cold panniculitis in children (Haxthausen's disease). Burns Incl Therm Inj. 1988
Feb;14(1):51-2.
530
Henry F, Letot B, Pierard-Franchimont C, Pierard GE. Winter skin diseases. [French]. Rev Med Liege. 1999
Nov;54(11):864-6.
531
Henry F, Letot B, Pierard-Franchimont C, Pierard GE. Winter skin diseases. [French]. Rev Med Liege. 1999
Nov;54(11):864-6.
532
Mahmoudi M. Cold-induced urticaria. J Am Osteopath Assoc. 2001 May;101(5 Suppl):S1-4.
533
Sarteel-Delvoye AM, Wiart T, Durier A. Chilblains. [French.] Rev Prat. 1998 Oct 1;48(15):1673-5.
534
Henry F, Letot B, Pierard-Franchimont C, Pierard GE. Winter skin diseases. [French]. Rev Med Liege. 1999
Nov;54(11):864-6.
535
Merlen JF. Chilblains. [French.] J Mal Vasc. 1986;11 Suppl A:28-31.
536
Vayssairat M. Chilblains. [French]. J Mal Vasc. 1992;17(3):229-31.
537
Viguier M, Pinquier L, Cavelier-Balloy B, de la Salmoniere P, Cordoliani F, Flageul B, Morel P, Dubertret L,
Bachelez H. Clinical and histopathologic features and immunologic variables in patients with severe chilblains. A
study of the relationship to lupus erythematosus. Medicine (Baltimore). 2001 May;80(3):180-8.
538
Viguier M, Pinquier L, Cavelier-Balloy B, de la Salmoniere P, Cordoliani F, Flageul B, Morel P, Dubertret L,
Bachelez H. Clinical and histopathologic features and immunologic variables in patients with severe chilblains. A
study of the relationship to lupus erythematosus. Medicine (Baltimore). 2001 May;80(3):180-8.
539
Duffill MB. Milkers' chilblains. N Z Med J. 1993 Mar 24;106(952):101-3.
540
Henry F, Letot B, Pierard-Franchimont C, Pierard GE. Winter skin diseases. [French]. Rev Med Liege. 1999
Nov;54(11):864-6.
541
Duffill MB. Milkers' chilblains. N Z Med J. 1993 Mar 24;106(952):101-3.
542
Bhalla A, Gupta S, Jain AP, Jajoo UN, Gupta OP, Kalantri SP. Blue toe syndrome: a rare complication of acute
pancreatitis. JOP. 2003 Jan;4(1):17-9.
543
Vayssairat M. Chilblains. [French]. J Mal Vasc. 1992;17(3):229-31.
544
Vayssairat M. Chilblains. [French]. J Mal Vasc. 1992;17(3):229-31.
545
Duffill MB. Milkers' chilblains. N Z Med J. 1993 Mar 24;106(952):101-3.
546
Rustin MH, Newton JA, Smith NP, Dowd PM. The treatment of chilblains with nifedipine: the results of a pilot
study, a double-blind placebo-controlled randomized study and a long-term open trial. Br J Dermatol. 1989
Feb;120(2):267-75.
547
Duffill MB. Milkers' chilblains. N Z Med J. 1993 Mar 24;106(952):101-3.
548
Vayssairat M. Chilblains. [French]. J Mal Vasc. 1992;17(3):229-31.
549
Larraz P, Ibarrola C. "Teruel feet". Care and treatment of frostbite wounds in the hospitals of Navarra during the
civil war. An Sist Sanit Navar. 2005 May-Aug;28(2):197-212.
550
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
551
Shepherd JT, Rusch NJ, Vanhoutte PM. Effect of cold on the blood vessel wall. Gen Pharmacol. 1983;14(1):61-
4.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
107
552
Gonzalez F, Leong K. Chapter 385 Cold-Induced Tissue Injuries. In Harwood-Nuss A, Wolfson AB, Linden CH,
Shepherd SM, Stenklyft PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and pressure-
related illness and injury. Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
553
Danielsson U. Windchill and the risk of tissue freezing. J Appl Physiol. 1996 Dec;81(6):2666-73.
554
Candler WH, Ivey H. Cold weather injuries among U.S. soldiers in Alaska: a five-year review. Mil Med. 1997
Dec;162(12):788-91.
555
Lehmuskallio E, Lindholm H, Koskenvuo K, Sarna S, Friberg O, Viljanen A. Frostbite of the face and ears:
epidemiological study of risk factors in Finnish conscripts. BMJ. 1995 Dec 23-30;311(7021):1661-3.
556
Reynolds K, Williams J, Miller C, Mathis A, Dettori J. Injuries and risk factors in an 18-day Marine winter
mountain training exercise. Mil Med. 2000 Dec;165(12):905-10.
557
Hashmi MA, Rashid M, Haleem A, Bokhari SA, Hussain T. Frostbite: epidemiology at high altitude in the
Karakoram mountains. Ann R Coll Surg Engl. 1998 Mar;80(2):91-5.
558
Taylor MS. Cold weather injuries during peacetime military training. Mil Med. 1992 Nov;157(11):602-4.
559
Reamy BV. Frostbite: review and current concepts. J Am Board Fam Pract. 1998 Jan-Feb;11(1):34-40.
560
Virokannas H, Anttonen H. Risk of frostbite in vibration-induced white finger cases. Arctic Med Res. 1993
Apr;52(2):69-72.
561
Cauchy E, Chetaille E, Marchand V, Marsigny B. Retrospective study of 70 cases of severe frostbite lesions: a
proposed new classification scheme. Wilderness Environ Med. 2001 Winter;12(4):248-55.
562
Daniels F, Jr. Contact cooling of the hand at -20° F. Technical Report EP-22. Quartermaster Research and
Development Center. US Army Natic, MA.
563
Hirvonen J. Some aspects on death in the cold and concomitant frostbites. Int J Circumpolar Health. 2000
Apr;59(2):131-6.
564
Candler WH, Ivey H. Cold weather injuries among U.S. soldiers in Alaska: a five-year review. Mil Med. 1997
Dec;162(12):788-91.
565
Naval Health Sciences Education and Training Command and Bureau of Medicine and Surgery. Clinical aspects
of cold weather NAVEDTRA 13147-A. Naval Education and Training Program Management Support Activity. July
1991.
566
Aygit AC, Sarikaya A. Imaging of frostbite injury by technetium-99m-sestamibi scintigraphy: a case report. Foot
Ankle Int. 2002 Jan;23(1):56-9.
567
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
568
Barker JR, Haws MJ, Brown RE, Kucan JO, Moore WD. Magnetic resonance imaging of severe frostbite
injuries. Ann Plast Surg. 1997 Mar;38(3):275-9.
569
Cauchy E, Chetaille E, Lefevre M, Kerelou E, Marsigny B. The role of bone scanning in severe frostbite of the
extremities: a retrospective study of 88 cases. Eur J Nucl Med. 2000 May;27(5):497-502.
570
Bhatnagar A, Sarker BB, Sawroop K, Chopra MK, Sinha N, Kashyap R. Diagnosis, characterisation and
evaluation of treatment response of frostbite using pertechnetate scintigraphy: a prospective study. Eur J Nucl Med
Mol Imaging. 2002 Feb;29(2):170-5.
571
Aygit AC, Sarikaya A. Imaging of frostbite injury by technetium-99m-sestamibi scintigraphy: a case report. Foot
Ankle Int. 2002 Jan;23(1):56-9.
572
Barker JR, Haws MJ, Brown RE, Kucan JO, Moore WD. Magnetic resonance imaging of severe frostbite
injuries. Ann Plast Surg. 1997 Mar;38(3):275-9.
573
Castellani JW, O’Brien C, Baker-Fulco C, Sawka MN, Young AJ. AD A395745 Technical note no. TN/02-2
Sustaining Health & Performance in Cold Weather Operations. US Army Research Institute of Environmental
Medicine, Natick. October, 2001.
574
Su CW, Lohman R, Gottlieb LJ. Frostbite of the upper extremity. Hand Clin. 2000 May;16(2):235-47.
575
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
576
Strohecker B, Parulski CJ. Frostbite injuries of the hand. Plast Surg Nurs 1997 Winter;17(4):212-6.
577
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
578
Punja K, Graham M, Cartotto R. Continuous infusion of epidural morphine in frostbite. J Burn Care Rehabil.
1998 Mar-Apr;19(2):142-5.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
108
579
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
580
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
581
Mills WJ Jr. Comments on this issue of Alaska Medicine--from then (1960) until now (1993). Alaska Med. 1993
Jan-Mar;35(1):70-87.
582
Kotel'nikov VP, Morozov VN. Neurohumoral regulation in frostbite [Russian]. Vestn Khir Im I I Grek. 1990
Feb;144(2):68-72.
583
Salimi Z, Wolverson MK, Herbold DR, Vas W, Salimi A. Treatment of frostbite with i.v. streptokinase: an
experimental study in rabbits.
AJR Am J Roentgenol. 1987 Oct;149(4):773-6.
584
Mills WJ Jr. Comments on this issue of Alaska Medicine--from then (1960) until now (1993). Alaska Med. 1993
Jan-Mar;35(1):70-87.
585
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
586
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
587
Twomey JA, Peltier GL, Zera RT. An open-label study to evaluate the safety and efficacy of tissue plasminogen
activator in treatment of severe frostbite. J Trauma. 2005 Dec;59(6):1350-4; discussion 1354-5.
588
McCauley RL, Heggers JP, Robson MC. Frostbite. Methods to minimize tissue loss. Postgrad Med. 1990
Dec;88(8):67-8, 73-7.
589
Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg [Am].
1981 Jan;6(1):43-7.
590
Heggers JP, Robson MC, Manavalen K, Weingarten MD, Carethers JM, Boertman JA, Smith DJ Jr, Sachs RJ.
Experimental and clinical observations on frostbite. Ann Emerg Med. 1987 Sep;16(9):1056-62.
591
McCauley RL, Heggers JP, Robson MC. Frostbite. Methods to minimize tissue loss. Postgrad Med. 1990
Dec;88(8):67-8, 73-7.
592
Heggers JP, Robson MC, Manavalen K, Weingarten MD, Carethers JM, Boertman JA, Smith DJ Jr, Sachs RJ.
Experimental and clinical observations on frostbite. Ann Emerg Med. 1987 Sep;16(9):1056-62.
593
Heggers JP, Robson MC, Manavalen K, Weingarten MD, Carethers JM, Boertman JA, Smith DJ Jr, Sachs RJ.
Experimental and clinical observations on frostbite. Ann Emerg Med. 1987 Sep;16(9):1056-62.
594
Greenwald D, Cooper B, Gottlieb L. An algorithm for early aggressive treatment of frostbite with limb salvage
directed by triple-phase scanning. Plast Reconstr Surg. 1998 Sep;102(4):1069-74.
595
Robson MC, Heggers JP. Evaluation of hand frostbite blister fluid as a clue to pathogenesis. J Hand Surg [Am].
1981 Jan;6(1):43-7.
596
Hayes DW Jr, Mandracchia VJ, Considine C, Webb GE. Pentoxifylline. Adjunctive therapy in the treatment of
pedal frostbite. Clin Podiatr Med Surg. 2000 Oct;17(4):715-22.
597
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
598
Duffill MB. Milkers' chilblains. N Z Med J. 1993 Mar 24;106(952):101-3.
599
Rustin MH, Newton JA, Smith NP, Dowd PM. The treatment of chilblains with nifedipine: the results of a pilot
study, a double-blind placebo-controlled randomized study and a long-term open trial. Br J Dermatol. 1989
Feb;120(2):267-75.
600
Naval Health Sciences Education and Training Command and Bureau of Medicine and Surgery. Clinical aspects
of cold weather NAVEDTRA 13147-A. Naval Education and Training Program Management Support Activity. July
1991.
601
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
602
Punja K, Graham M, Cartotto R. Continuous infusion of epidural morphine in frostbite. J Burn Care Rehabil
1998 Mar-Apr;19(2):142-5.
603
Koster U, Mutschler B, Hempel V. Treatment of frostbite of the extremities by combined axillary plexus and
peridural anesthesia: a case report including blood levels of bupivacaine. [German]. Reg Anaesth. 1987
Jul;10(3):93-5.
604
Taylor MS. Lumbar epidural sympathectomy for frostbite injuries of the feet. Mil Med. 1999 Aug;164(8):566-7.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
109
605
Bouwman DL, Morrison S, Lucas CE, Ledgerwood AM. Early sympathetic blockade for frostbite--is it of value?
J Trauma. 1980 Sep;20(9):744-9.
606
von Heimburg D, Noah EM, Sieckmann UP, Pallua N. Hyperbaric oxygen treatment in deep frostbite of both
hands in a boy. Burns. 2001 Jun;27(4):404-8.
607
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
608
Foray J. Mountain frostbite. Current trends in prognosis and treatment (from results concerning 1261 cases). Int J
Sports Med 1992 Oct;13 Suppl 1:S193-6.
609
Naval Health Sciences Education and Training Command and Bureau of Medicine and Surgery. Clinical aspects
of cold weather NAVEDTRA 13147-A. Naval Education and Training Program Management Support Activity. July
1991.
610
Luisto M. Unusual and iatrogenic sources of tetanus. Ann Chir Gynaecol. 1993;82(1):25-9.
611
Valnicek SM, Chasmar LR, Clapson JB. Frostbite in the prairies: a 12-year review. Plast Reconstr Surg. 1993
Sep;92(4):633-41.
612
Page RE, Robertson GA. Management of the frostbitten hand. Hand. 1983 Jun;15(2):185-91.
613
Ervasti O, Hassi J, Rintamaki H, Virokannas H, Kettunen P, Pramila S, Linna T, Tolonen U, Manelius J.
Sequelae of moderate finger frostbite as assessed by subjective sensations, clinical signs, and thermophysiological
responses. Int J Circumpolar Health. 2000 Apr;59(2):137-45.
614
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
615
Wrenn K. Immersion foot. A problem of the homeless in the 1990s. Arch Intern Med. 1991 Apr;151(4):785-8.
616
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
617
Teixeira F, Pollock M, Karim A, Jiang Y. Use of antioxidants for the prophylaxis of cold-induced peripheral
nerve injury. Mil Med. 2002 Sep;167(9):753-5.
618
Ramstead KD, Hughes RG, Webb AJ. Recent cases of trench foot. Postgrad Med J. 1980 Dec;56(662):879-83.
619
Castellani JW, O’Brien C, Baker-Fulco C, Sawka MN, Young AJ. AD A395745 Technical note no. TN/02-2
Sustaining Health & Performance in Cold Weather Operations. US Army Research Institute of Environmental
Medicine, Natick. October, 2001.
620
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994:64.
621
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
622
Castellani JW, O’Brien C, Baker-Fulco C, Sawka MN, Young AJ. AD A395745 Technical note no. TN/02-2
Sustaining Health & Performance in Cold Weather Operations. US Army Research Institute of Environmental
Medicine, Natick. October, 2001.
623
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
624
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
625
Irwin MS. Nature and mechanism of peripheral nerve damage in an experimental model of non-freezing cold
injury. Ann R Coll Surg Engl. 1996 Jul;78(4):372-9.
626
Irwin MS, Sanders R, Green CJ, Terenghi G. Neuropathy in non-freezing cold injury (trench foot). J R Soc Med.
1997 Aug;90(8):433-8.
627
Teixeira F, Pollock M, Karim A, Jiang Y. Use of antioxidants for the prophylaxis of cold-induced peripheral
nerve injury. Mil Med. 2002 Sep;167(9):753-5.
628
Wrenn K. Immersion foot. A problem of the homeless in the 1990s. Arch Intern Med. 1991 Apr;151(4):785-8.
629
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
630
Adnot J, Lewis CW. Chapter 4 immersion foot syndromes. In Zajtchuk, ed. Textbook of Military Medicine:
Military Dermatology. Office of the Surgeon General, Department of the Army, Falls Church, 1994.
631
Ahle NW, Buroni JR, Sharp MW, Hamlet MP. Infrared thermographic measurement of circulatory compromise
in trenchfoot-injured Argentine soldiers. Aviat Space Environ Med. 1990 Mar;61(3):247-50.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
110
632
Chen GS, Yu HS, Yang SA, Chen SS. Responses of cutaneous microcirculation to cold exposure and neuropathy
in vibration-induced white finger. Microvasc Res. 1994 Jan;47(1):21-30.
633
Stedman’s Medical Dictionary Version 1.5. WordPerfect Corporation. 1993. Based on Stedman’s Medical
Dictionary, 25
th
Edition. Williams & Wilkins. 1994.
634
Creager, MA. XVI Peripheral arterial disease. 1 Cardiovascular medicine. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York, May 1998.
635
Creager, MA. XVI Peripheral arterial disease. 1 Cardiovascular medicine. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York. May 1998.
636
Schrier SL. IV Hemoglobinopathies and hemolytic anemias. 5 Hematology. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York. April 1999.
637
Escoda L, Pereira A, Graena A, Vives-Corrons JL, Rozman C. Paroxysmal cold hemoglobinuria: only in the
textbooks? [Spanish.] Med Clin (Barc). 1991 Mar 23;96(11):419-21.
638
Schrier SL. IV Hemoglobinopathies and hemolytic anemias. 5 Hematology. SAM-CD Connected®. Dale DC,
Federman DD, Eds. WebMD Corporation, New York. April 1999.
639
Longstreth J, de Gruijl FR, Kripke ML, Abseck S, Arnold F, Slaper HI, Velders G, Takizawa Y, van der Leun
JC. Health risks. J Photochem Photobiol B. 1998 Oct;46(1-3):20-39.
640
Johnson GJ. Aetiology of spheroidal degeneration of the cornea in Labrador. Br J Ophthalmol. 1981
Apr;65(4):270-83.
641
Dahan E, Judelson J, Welsh NH. Regression of Labrador keratopathy following cataract extraction. Br J
Ophthalmol. 1986 Oct;70(10):737-41.
642
Johnson GJ, Green JS, Paterson GD, Perkins ES. Survey of ophthalmic conditions in a Labrador community: II.
Ocular disease. Can J Ophthalmol. 1984 Aug;19(5):224-33.
643
Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: do ophthalmic nonsteroidal anti-
inflammatory drugs reduce the pain associated with simple corneal abrasion without delaying healing?
Ann Emerg Med. 2003 Jan;41(1):134-40.
644
Daxer A, Blumthaler M, Schreder J, Ettl A. Effectiveness of eye drops protective against ultraviolet radiation.
Ophthalmic Res. 1998;30(5):286-90.
645
Kolstad A, Opsahl R Jr. Cold injury to corneal epithelium. A cause of blurred vision in cross-country skiers. Acta
Ophthalmol (Copenh). 1969;47(3):656-9.
646
Dorland WA. Dorland's Illustrated Medical Dictionary, 29th Edition. W. B. Saunders, Philadelphia. 2000.
647
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
648
Simmons EH, O'Driscoll SW, Gamarra JA. Clinical and experimental evidence for the use of hypothermia in
decompression sickness. Aviat Space Environ Med. 1982 Mar;53(3):266-8.
649
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
650
Jones BH, chair, DoD Injury Surveillance and Prevention Work Group. Atlas of injuries in the U.S. armed forces.
A report by the Department of Defense Injury Surveillance and Prevention Work Group for the Assistant Deputy
Under Secretary of Defense for Safety and Occupational Health. Supplement to Military Medicine, International
Journal of AMSUS, vol 164, no 8. DoD Injury Surveillance and Prevention Work Group. August 1999.
651
CDC. Current Trends Hypothermia -- United States. MMWR Weekly. Centers for Disease Control and
Prevention Morbidity and Mortality Weekly Report. United States Department of Health and Human Services
Centers for Disease Control and Prevention. January 28, 1983 / 32(3);46-8.
652
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
653
CDC. Current Trends Hypothermia -- United States. MMWR Weekly. Centers for Disease Control and
Prevention Morbidity and Mortality Weekly Report. United States Department of Health and Human Services
Centers for Disease Control and Prevention. January 28, 1983 / 32(3);46-8.
654
Hoffman RG, Pozos RS. Experimental hypothermia and cold perception. Aviat Space Environ Med. 1989
Oct;60(10 Pt 1):964-9.
655
Keatinge WR, Mason AC, Millard CE, Newstead CG. Effects of fluctuating skin temperature on
thermoregulatory responses in man. J Physiol. 1986 Sep;378:241-52.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
111
656
Herr RD, White GL Jr. Hypothermia: threat to military operations. Mil Med. 1991 Mar;156(3):140-4.
657
Irwin BR. A case report of hypothermia in the wilderness. Wilderness Environ Med. 2002 Summer;13(2):125-8.
658
Herr RD, White GL Jr. Hypothermia: threat to military operations. Mil Med. 1991 Mar;156(3):140-4.
659
Ballester JM, Harchelroad FP. Hypothermia: an easy-to-miss, dangerous disorder in winter weather.
Geriatrics. 1999 Feb;54(2):51-2, 55-7.
660
Olsen DH, Gothgen IH. Treatment of accidental hypothermia. [Danish.] Ugeskr Laeger. 2000 Sep
4;162(36):4790-4.
661
Choudhary SP, Bajaj RK, Gupta RK. Knowledge, attitude and practices about neonatal hypothermia among
medical and paramedical staff. Indian J Pediatr. 2000 Jul;67(7):491-6.
662
Fisher A, Foex P, Emerson PM, Darley JH, Rauscher LA. Oxygen availability during hypothermic
cardiopulmonary bypass. Crit Care Med. 1977 May-Jun;5(3):154-8.
663
Bacher A, Illievich UM, Fitzgerald R, Ihra G, Spiss CK. Changes in oxygenation variables during progressive
hypothermia in anesthetized patients. J Neurosurg Anesthesiol. 1997 Jul;9(3):205-10.
664
Danzl DF, Pozos RS. Accidental hypothermia. N Engl J Med. 1994 Dec 29;331(26):1756-60.
665
Danzl DF, Pozos RS. Accidental hypothermia. N Engl J Med. 1994 Dec 29;331(26):1756-60.
666
De Souza D, Riera AR, Bombig MT, Francisco YA, Brollo L, Filho BL, Dubner S, Schapachnik E, Povoa R.
Electrocardiographic changes by accidental hypothermia in an urban and a tropical region. J Electrocardiol. 2007
Jan;40(1):47-52. Epub 2006 Oct 5.
667
CDC. Hypothermia-Related Deaths --- Philadelphia, 2001, and United States, 1999. MMWR Weekly. Centers for
Disease Control and Prevention Morbidity and Mortality Weekly Report. United States Department of Health and
Human Services Centers for Disease Control and Prevention. February 7, 2003 / 52(05);86-87.
668
Locher T, Walpoth B, Pfluger D, Althaus U. Accidental hypothermia in Switzerland (1980-1987)--case reports
and prognostic factors. [German]. Schweiz Med Wochenschr. 1991 Jul 9;121(27-28):1020-8.
669
Vaagenes P. Accidental hypothermia. [Swedish]. Tidsskr Nor Laegeforen. 1993 Aug 30;113(20):2579-82.
670
Currier JJ. Chapter 386 hypothermia. In Harwood-Nuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft
PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and pressure- related illness and injury.
Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
671
Locher T, Walpoth B, Pfluger D, Althaus U. Accidental hypothermia in Switzerland (1980-1987)--case reports
and prognostic factors. [German]. Schweiz Med Wochenschr. 1991 Jul 9;121(27-28):1020-8.
672
Dobson JA, Burgess JJ. Resuscitation of severe hypothermia by extracorporeal rewarming in a child. J Trauma.
1996 Mar;40(3):483-5.
673
Vassal T, Benoit-Gonin B, Carrat F, Guidet B, Maury E, Offenstadt G. Severe accidental hypothermia treated in
an ICU: prognosis and outcome. Chest. 2001 Dec;120(6):1998-2003.
674
Olsen DH, Gothgen IH. Treatment of accidental hypothermia. [Danish.] Ugeskr Laeger. 2000 Sep
4;162(36):4790-4.
675
Delaney KA, Vassallo SU, Larkin GL, Goldfrank LR. Rewarming rates in urban patients with hypothermia:
prediction of underlying infection. Acad Emerg Med. 2006 Sep;13(9):913-21.
676
Ghawche F, Destee A. Hypothermia and multiple sclerosis. A case with 3 episodes of transient hypothermia.
[French.] Rev Neurol (Paris). 1990;146(12):767-9.
677
Linker RA, Mohr A, Cepek L, Gold R, Prange H. Core hypothermia in multiple sclerosis: case report with
magnetic resonance imaging localization of a thalamic lesion. Mult Scler. 2006 Feb;12(1):112-5.
678
de Tollenaer SM, Buysse C, van den Anker JN, Touw DJ, de Hoog M. Life threatening central nervous system
manifestations and hypothermia due to maneb intoxication in a child: a case report. Ther Drug Monit. 2006
Dec;28(6):813-5.
679
Hemelsoet DM, De Bleecker JL. Post-traumatic spontaneous recurrent hypothermia: a variant of Shapiro's
syndrome. Eur J Neurol. 2007 Feb;14(2):224-7.
680
Currier JJ. Chapter 386 hypothermia. In Harwood-Nuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft
PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and pressure- related illness and injury.
Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
681
Knobel B, Mikhlin A. Severe accidental hypothermia in an elderly woman. [Hebrew.] Harefuah. 2001
Nov;140(11):1014-7, 1119.
682
Kallman H. Protecting your elderly patient from winter's cold. Geriatrics. 1985 Dec;40(12):69-72, 77, 81.
683
Meert AP, Berghmans T, Sculier JP. Hypothermia and Hodgkin's disease: case report and review of the literature.
Acta Clin Belg. 2006 Sep-Oct;61(5):252-4.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
112
684
Prusaczyk WK, Sawka MN. Effects of pyridostigmine bromide on human thermoregulation during cold water
immersion. J Appl Physiol. 1991 Aug;71(2):432-7.
685
Passias TC, Mekjavic IB, Eiken O. The effect of 30% nitrous oxide on thermoregulatory responses in humans
during hypothermia. Anesthesiology. 1992 Apr;76(4):550-9.
686
Bourdon L, Jacobs I, Bell D, Ducharme MB. Effect of triazolam on responses to a cold-water immersion in
humans. Aviat Space Environ Med. 1995 Jul;66(7):651-5.
687
Vitezic D, Rozmanic V, Franulovic J, Ahel V, Matesic D. Naphazoline nasal drops intoxication in children. Arh
Hig Rada Toksikol. 1994 Mar;45(1):25-9.
688
Abu-Qare AW, Abou-Donia MB. Sarin: health effects, metabolism, and methods of analysis. Food Chem
Toxicol. 2002 Oct;40(10):1327-33.
689
Budd GM, Hendrie AL, Jeffery SE. Behavioural temperature regulation during a motor-toboggan traverse in
Antarctica. Eur J Appl Physiol Occup Physiol. 1986;55(5):507-16.
690
Young AJ, O'Brien C, Sawka MN, Gonzalez RR. Physiological problems associated with wearing NBC
protective clothing during cold weather. Aviat Space Environ Med. 2000 Feb;71(2):184-9.
691
Tom PA, Garmel GM, Auerbach PS. Environment-dependent sports emergencies. Med Clin North Am. 1994
Mar;78(2):305-25.
692
Ballester JM, Harchelroad FP. Hypothermia: an easy-to-miss, dangerous disorder in winter weather.
Geriatrics. 1999 Feb;54(2):51-2, 55-7.
693
Vaagenes P. Accidental hypothermia. [Swedish]. Tidsskr Nor Laegeforen. 1993 Aug 30;113(20):2579-82.
694
Kornberger E, Mair P. Important aspects in the treatment of severe accidental hypothermia: the Innsbruck
experience. J Neurosurg Anesthesiol. 1996 Jan;8(1):83-7.
695
Harnett RM, O'Brien EM, Sias FR, Pruitt JR. Initial treatment of profound accidental hypothermia.
Aviat Space Environ Med. 1980 Jul;51(7):680-7.
696
Splittgerber FH, Talbert JG, Sweezer WP, Wilson RF. Partial cardiopulmonary bypass for core rewarming in
profound accidental hypothermia. Am Surg. 1986 Aug;52(8):407-12.
697
Hayward JS, Eckerson JD, Kemna D. Thermal and cardiovascular changes during three methods of resuscitation
from mild hypothermia. Resuscitation. 1984 Feb;11(1-2):21-33.
698
Vaagenes P. Accidental hypothermia. [Swedish]. Tidsskr Nor Laegeforen. 1993 Aug 30;113(20):2579-82.
699
Hayward JS, Steinman AM. Accidental hypothermia: an experimental study of inhalation rewarming. Aviat
Space Environ Med. 1975 Oct;46(10):1236-40.
700
Sterba JA. Efficacy and safety of prehospital rewarming techniques to treat accidental hypothermia. Ann Emerg
Med. 1991 Aug;20(8):896-901.
701
Harnett RM, O'Brien EM, Sias FR, Pruitt JR. Initial treatment of profound accidental hypothermia.
Aviat Space Environ Med. 1980 Jul;51(7):680-7.
702
Olsen DH, Gothgen IH. Treatment of accidental hypothermia. [Danish]. Lakartidningen. 2000 Nov
1;97(44):4992-7.
703
Vella J, Farrell J, Leavey S, Magee C, Carmody M, Walshe J. The rapid reversal of profound hypothermia using
peritoneal dialysis. Ir J Med Sci. 1996 Apr-Jun;165(2):113-4.
704
Owda A, Osama S. Hemodialysis in management of hypothermia. Am J Kidney Dis. 2001 Aug;38(2):E8.
705
Nuckton TJ, Claman DM, Goldreich D, Wendt FC, Nuckton JG. Hypothermia and afterdrop following open
water swimming: the Alcatraz/San Francisco Swim Study. Am J Emerg Med. 2000 Oct;18(6):703-7.
706
Nuckton TJ, Claman DM, Goldreich D, Wendt FC, Nuckton JG. Hypothermia and afterdrop following open
water swimming: the Alcatraz/San Francisco Swim Study. Am J Emerg Med. 2000 Oct;18(6):703-7.
707
Lloyd EL. The cause of death after rescue. Int J Sports Med. 1992 Oct;13 Suppl 1:S196-9.
708
Splittgerber FH, Talbert JG, Sweezer WP, Wilson RF. Partial cardiopulmonary bypass for core rewarming in
profound accidental hypothermia. Am Surg. 1986 Aug;52(8):407-12.
709
Splittgerber FH, Talbert JG, Sweezer WP, Wilson RF. Partial cardiopulmonary bypass for core rewarming in
profound accidental hypothermia. Am Surg. 1986 Aug;52(8):407-12.
710
Danzl DF, Pozos RS. Accidental hypothermia. N Engl J Med. 1994 Dec 29;331(26):1756-60.
711
Long WB. Cardiopulmonary bypass for rewarming profound hypothermia patients. Presented at the Critical
Decisions in Hypothermia Annual International Forum, Portland, Oreg., February 27, 1992. Referenced by Danzl
DF, Pozos RS. Accidental hypothermia. N Engl J Med. 1994 Dec 29;331(26):1756-60.
712
Danzl DF, Pozos RS. Accidental hypothermia. N Engl J Med. 1994 Dec 29;331(26):1756-60.
713
Cummins RO, ed. ACLS Provider Manual. Copyright © 2001 American Heart Association, Dallas. 75.
NEHC-TM-OEM 6260.6A Prevention and Treatment of Heat and Cold Stress Injuries
113
714
Orts A, Alcaraz C, Delaney KA, Goldfrank LR, Turndorf H, Puig MM. Bretylium tosylate and electrically
induced cardiac arrhythmias during hypothermia in dogs. Am J Emerg Med. 1992 Jul;10(4):311-6.
715
Elenbaas RM, Mattson K, Cole H, Steele M, Ryan J, Robinson W. Bretylium in hypothermia-induced ventricular
fibrillation in dogs. Ann Emerg Med. 1984 Nov;13(11):994-9.
716
Currier JJ. Chapter 386 hypothermia. In Harwood-Nuss A, Wolfson AB, Linden CH, Shepherd SM, Stenklyft
PH, eds. The Clinical Practice of Emergency Medicine Part II cold-, heat-, and pressure- related illness and injury.
Copyright © 2001 Lippincott Williams & Wilkins, Philadelphia.
717
Wollenek G, Honarwar N, Golej J, Marx M. Cold water submersion and cardiac arrest in treatment of severe
hypothermia with cardiopulmonary bypass. Resuscitation. 2002 Mar;52(3):255-63.
718
Brugger H, Durrer B, Adler-Kastner L. On-site triage of avalanche victims with asystole by the emergency
doctor. Resuscitation. 1996 Feb;31(1):11-6.
719
Mair P, Kornberger E, Furtwaengler W, Balogh D, Antretter H. Prognostic markers in patients with severe
accidental hypothermia and cardiocirculatory arrest. Resuscitation. 1994 Jan;27(1):47-54.
720
Brugger H, Durrer B, Adler-Kastner L. On-site triage of avalanche victims with asystole by the emergency
doctor. Resuscitation. 1996 Feb;31(1):11-6.
721
Farbrot K, Husby P, Andersen KS, Grong K, Farstad M, Koller ME. Rewarming of patients with accidental
hypothermia with the help of heart-lung machine. [Norwegian.] Tidsskr Nor Laegeforen. 2000 Jun 20;120(16):1854-
7.
722
Hirvonen J. Some aspects on death in the cold and concomitant frostbites. Int J Circumpolar Health. 2000
Apr;59(2):131-6.
723
Schulman H, Laufer L, Berginer J, Hershkowitz E, Berenstein T, Sofer S, Maor E, Hertzanu Y. CT findings in
neonatal hypothermia. Pediatr Radiol. 1998 Jun;28(6):414-7.
724
Robinson MD, Seward PN. Submersion injury in children. Pediatr Emerg Care. 1987 Mar;3(1):44-9.
725
Flores-Maldonado A, Medina-Escobedo CE, Rios-Rodriguez HM, Fernandez-Dominguez R. Mild perioperative
hypothermia and the risk of wound infection. Arch Med Res. 2001 May-Jun;32(3):227-31.
726
Splittgerber FH, Talbert JG, Sweezer WP, Wilson RF. Partial cardiopulmonary bypass for core rewarming in
profound accidental hypothermia. Am Surg. 1986 Aug;52(8):407-12.
727
Walpoth BH, Walpoth-Aslan BN, Mattle HP, Radanov BP, Schroth G, Schaeffler L, Fischer AP, von Segesser L,
Althaus U. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal
blood warming. N Engl J Med. 1997 Nov 20;337(21):1500-5.
728
Kornberger E, Mair P. Important aspects in the treatment of severe accidental hypothermia: the Innsbruck
experience. J Neurosurg Anesthesiol. 1996 Jan;8(1):83-7.
729
Walpoth BH, Walpoth-Aslan BN, Mattle HP, Radanov BP, Schroth G, Schaeffler L, Fischer AP, von Segesser L,
Althaus U. Outcome of survivors of accidental deep hypothermia and circulatory arrest treated with extracorporeal
blood warming. N Engl J Med. 1997 Nov 20;337(21):1500-5.
730
Fox JB, Thomas F, Clemmer TP, Grossman M. A retrospective analysis of air-evacuated hypothermia patients.
Aviat Space Environ Med. 1988 Nov;59(11 Pt 1):1070-5.
731
McAlpine CH, Dall JL. Outcome after episodes of hypothermia. Age Ageing. 1987 Mar;16(2):115-8.
732
Levi S, Taylor W, Robinson LE, Levy LI. Analysis of morbidity and outcome of infants weighing less than 800
grams at birth. South Med J. 1984 Aug;77(8):975-8.
733
Sofer S, Benkovich E. Severe infantile hypothermia: short- and long-term outcome. Intensive Care Med. 2000
Jan;26(1):88-92.
734
Kangas E, Niemela H, Kojo N. Treatment of hypothermic circulatory arrest with thoracotomy and pleural lavage.
Ann Chir Gynaecol. 1994;83(3):258-60.
735
U.S. Navy. OPNAV Instruction 5100.23F Navy Occupational Safety and health (NAVOSH) Program Manual.
U.S. Navy Chief of Naval Operations. 15 July 2002.
736
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