Heat Stroke & Heat Related Illness

Environmental Illnesses such as Heat Stoke and Hypothermia are entirely preventable.  Casualties with either of these conditions are usually a result of:

Inappropriate equipment

Lack of education

Bad planning

 

These casualties should be those who you happen upon or are called to.  No one in your group should ever be a casualty of environmental illness.

 

Physiology

The hypothalamus is responsible for ensuring the core temperature stays within a very narrow margin of normal temperature by initiating physiological responses to keep the heat in or let heat out.   Heat Related Illnesses occur as a result of either the physiological effects of prolonged compensatory mechanisms which regulate core temperature (such as sweating) or the cessation of these mechanisms.
 

Contributory Factors

Metabolism

Just being alive generates heat.

Exertion

Movement generates heat:  If we are active we are increasing heat generation.

Environment

Lying motionless and unclothed in an ambient temperature of 28oc or below, we will lose heat by radiation faster than we can generate it.(1)   In temperatures above this we will generate heat faster than we can radiate it.

Sweating is a normal response to a rise in core temperature.  The vaporisation of 1.7mL of sweat consumes 1 kcal of heat.(2)  In tropical conditions with high humidity sweating becomes less effective.

Drugs

Certain drugs can increase the risk of heat related illness by either the generation of heat by the drugs metabolic actions or by inhibiting thermoregulation.  Common drugs which may impair heat regulation include: (3)

  • Anticholinergics
  • Antihistamines
  • Antipsychotics
  • Benzodiazepines
  • Beta-blockers
  • Calcium-channel blockers

 

  • Diuretics
  • Laxatives
  • Neuroleptics
  • Phenothiazines
  • Thyroid agonists
  • Tricyclic antidepressants

 

Fitness

Several studies have linked an increased risk of heat-related illness with overweight or obese casualties.(4, 5)

Individuals with high levels of cardiopulmonary fitness tolerate more activity and acclimatize to hot conditions more rapidly than those without as a result of increased sweat volumes and higher subjective tolerance for activity when hyperthermic.

Gender

Gender is not a factor; neither males nor females tolerate heat better or worse than another.  Heat tolerances are correlated more closely to body mass index rather than gender.(6) 

 

Prevention

Acclimatisation is key to prevention; 1 to 2 hours of heat-exposed exertion per day over 10 to 14 days results in reproducible adaptations that increase the body’s ability to tolerate and remove heat. (7-9)  These adaptations may persist for up to a month (10) but evidence suggests that a bout of heat stroke may acutely reset these thermoregulatory adaptations and cause elevated risk for subsequent heat injury for months after the initial event. (11)

Hyper-hydration before activity has not been shown to have a significant effect on heat tolerance, nor has active body cooling before activity. (12)

 

Minor Heat Illnesses

Heat Cramps

Heat cramps typically develop at rest or at night.  Given the cause is usually low potassium brought on by dehydration, the treatment is simply rehydration with ORS - or if possible – water supplemented with potassium rich food such as spinach, dried apricots, mushrooms and bananas.

Heat Oedema

Swelling, especially of the lower limbs and hands due to inter-cellular fluid retention.  This is a benign condition without serious consequence.   Increased vasodilation increases permeability of the vessel walls accelerated by an imbalance of salts associated with dehydration.

Recovery is usually rapid with rest, rehydration and elevation of the affected limbs and compression stockings.  Mobility – but not strenuous exercise – will help.

Heat Syncope

Syncope (pronounces sing-co-pee) or ‘fainting’ is a transient loss of consciousness brought on by several factors triggered by heat exposure and or exertion.  Recovery is normally quick and accelerated by rest, rehydration and a return to milder environment.  Contributing factors include advanced age, prolonged standing, dehydration, medication and existing medical conditions.

Initial treatment is assessment and stabilisation of the ABCs in a cool environment.

Heat Exhaustion and Heat Stroke

An increase in blood temperature by less than 1oC triggers the hypothalamus to increase blood flow to the skin by up to 8L/min via vasodilation.  As blood is shunted to the skin to increase radiative  heat loss, perfusion to the core is reduced. (13)

The subsequent reduction in Basal Metabolic Rate also decreases heat production. 

If the heat is sufficiently intense, a release of acetylcholine  (ACh) stimulates sweating causing evaporative heat loss.

Sweating will continue as long as sufficient water is available.  As the availability of free water diminishes two physiological responses are triggered:

  • In an attempt to reclaim free water, the body will begin to release vasopressin.  Prolonged reclamation of free water out of proportion to sodium intake may result in haemodilution and hyponatremia (low sodium) contributing to heat cramps.
     
  • In response to hypovolemia as a result of fluid loss, extended dependence on aldosterone (which regulates blood pressure) can cause hypokalaemia (low potassium) that in turn may also lead to heat cramps.

Both hyponatraemia and hypokalaemia can develop into life-threatening medical emergencies. (14)

 

The distinction between Heat Exhaustion and Heat Stoke is often cited as (3):

Heat Exhaustion: Core temperature greater than 37oC but less than 40oC

Heat Stroke:  Core temperature >40oC

A digital fridge thermometer is an ideal thermometer in a remote environment being small, cheap and non-invasive.  Placed in the armpit of the casualty this can constantly monitor the casualty’s temperature.  Axillary temperature is typically 1­­.5oC less than core temperature (15).

When a thermometer is not available a significant – and life threatening - sign is the cessation of sweating.  This indicates that not only is the casualty dehydrated to the point they have lost the ability to reclaim available water for sweating but also that the casualty no longer has the ability to regulate their own temperature through evaporative heat loss.   Left untreated the casualty’s temperature is likely to rise until the point of death.

 

Dehydration              

Dehydration impairs thermoregulatory and cardiovascular performance.   The method of rehydration may sometimes depend on the cause of the dehydration.

Water is appropriate but a rehydration solution is preferred.   This may be a commercially available Oral Rehydration Solution (ORS) such as Dioralyte, a sports supplement such as SIS Hydro or a simple homemade formula.  The World Health Organisation recommend:

  • 30g (6 teaspoons) sugar
  • 2.5g (half teaspoon) salt.
  • 1 Litre clean water
     

For prolonged care, have the casualty pass urine hourly and compare volume, clarity and colour.  Hydration is achieved when the casualty can pass one litre or more of pale, clear urine over 24 hours.

For the unconscious - or desperate - casualty, consider rectal rehydration.

 

Treatment

Passive cooling

Move the casualty to the shade and loosen clothing to increase air-flow over the casualty and aid convective heat loss.


Hydration

Hydration is an important factor in reducing hyperthermia.(16, 17)  Using the guidelines above for dehydration, encourage small sips rather than gulping as much as possible as quickly as possible.  If the casualty has a reduced level of consciousness, consider rectal rehydration.

Efforts to hydrate the casualty should not delay whole body cooling of the casualty.(18)

Cold Water Immersion

The historic concern is that Cold Water Immersion (CWI) causes vasoconstriction and shivering which both inhibit heat loss.  Although CWI may cause shivering if immersed for more than 10 minutes, water transfers heat up to 24 times faster than air (19) and ice water cooling has been shown to be doubly effective than spraying water over the body to aid evaporative cooling (0.2oC/min versus 0.11oC/min).(20)

The practicalities of CWI make this treatment sometimes unfeasible in the field; requiring a bath or large body of water to immerse the casualty’s limbs and torso, but not head!  The danger of CWI is the risk of drowning and / or currents so standard water safety principles should be maintained, especially if the casualty has a reduced level of consciousness. 

There is no physiological risk to immersing a casualty with heat stroke.(21)

Evaporative cooling

If Cold Water Immersion is not possible, begin evaporative cooling as quickly as possible; remove all but the first layer of clothing and saturate with water.  Aid evaporative cooling with fanning to increase convective heat losses.  These techniques can achieve heat losses of 0.8-0.4oC per miute.(22)

There is little benefit in stripping the casualty naked as the clothing will hold a greater amount of water, increasing the capacity for heat transfer.  Excess water will simply run off the naked casualty’s skin and be lost to the ground.

Ice Packs

There is minimal evidence that Ice Packs (or chemical cold packs) reduce temperature when applied strategically in the armpit, groin and behind the neck but have marked results when covering the whole body.(23, 24)

Medications

Some medications have antipyretic properties (including aspirin and paracetamol) which are useful in reducing fever from infection but no medications exist which pharmacologically reduce temperature from exertional Heat Stroke.(25, 26)

One last thought

Environmental Illnesses affect everyone:  If one member of your group is exhibiting signs of heat illness, treat everyone in the group.  If one person is hyperthermic, everyone one else is likely to become hyperthermic as all members have been exposed to the same environment so they are all treated preemptively.   Stop for a rest, take on more food and drink, remove clothing and make sure everyone is happy before continuing with the activity.

Related Article - Hypothermia Guidelines

 

References

  1. Wlkerson JA (Ed)  (1998)  Medicine for Mountaineering & Other Wilderness Activities.  The Mountaineers.  Seattle.  p300
     
  2. Nelson NA, Eichna LW, Horvath SM, Shelley WB. (1947)  “Thermal exchanges of man at high temperatures”.  American Journal of Physiology.  151:626–652
     
  3. Lipman GS,  Eifling KP,  Ellis MA,  Gaudio FG, Otten EM, Grissom CK(2014)  “Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Heat-Related Illness: 2014 Update”, Wilderness & Environmental Medicine. 25, S55–S65
     
  4. Bedno SA, Li Y, Han W, etal.  (2010)  “Exertional heat illnessamongoverweight U.S. Army recruits in basic training”.  Aviation, Space, and Environmental Medicine.  81:107–111.
     
  5. Epstein Y, Moran DS, Shapiro Y, Sohar E, ShemerJ.  (1999)  “Exertional heat stroke: a case series”.  Medicine & Science in Sports & Exercise.  31:224–228.
     
  6. Lemire B, Gagnon D, Jay O, Dorman L, Du Charme MB, Kenny GP.  (2008)  “Influence of adiposity on cooling efficiency in hyperthermic individuals”.  European Journal of Applied Physiology.  104: 67–74.
     
  7. Brazaitis M, Skurvydas A.  (2010)  “Heat acclimation does not reduce the impact of hyperthermia on central fatigue”.  European Journal of Applied Physiology.  109:771–778.
     
  8. Cheung SS, McLellan TM.  (1998)  “Heat acclimation, aerobic fitness, and hydration effects on tolerance during uncompensable heatstress”.  Journal of Applied Physiology.  84:1731–1739.
     
  9. Garrett AT, Goosens NG, Rehrer NJ, Patterson MJ, Cotter JD.  (2009)  “Induction and decay of short-term heat acclimation”.  European Journal of Applied Physiology.  107:659–670.
     
  10. Weller AS, Linnane DM, Jonkman AG, Daanen HA.  (2007)  “Quantification of the decay and re-induction of heat acclimation in dry-heat following 12 and 26 days without exposure to heat stress”. European Journal of Applied Physiology.   102:57–66.
     
  11. Armstrong LE, De Luca JP, Hubbard RW.  (1990)  “Time course of recovery and heat acclimation ability of prior exertional heat stroke patients”.  Medicine & Science in Sports & Exercise.  22:36–48.
     
  12. DuffieldR, Steinbacher G, Fairchild TJ.  (2009)  “The use of mixed-method, part-body pre-cooling procedures for team-sport athletes training in the heat”.  Journal of Strength & Conditioning Research.  23:2524–2532.
     
  13. Rowell LB.  (1983)  “Cardiovascular aspects of human thermoregulation”.  Circulation Research.  52:367–379.
     
  14. American Heart Association (2005)  “Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care”.  Part 10.1: Life-Threatening Electrolyte Abnormalities.  Circulation.  112: IV-121-IV-125
     
  15. Sund-Levander M, Forsberg C andKarin Wahren L.  (2002) “Normal oral, rectal, tympanic and axillary body temperature in adult men and women: a systematic literature review”. Scandinavian Journal of Caring Sciences. Vol. 16 No. 2: 122
     
  16. González-Alonso J, Calbet JA, Nielsen B.  (1999)  “Metabolic and thermodynamic responses to dehydration-induced reductions in muscle blood flow in exercising humans”.  Journal of Physiology.  520 (Pt2):577–589.
     
  17. Casa DJ, Armstrong LE, Hillman SK, etal.  (2000)  “National Athletic Trainers’ Association Position Statement:  Fluid replacement for athletes”.  Journal of Athletic Training.  35:212–224.
     
  18. Hostler D, Reis SE, Bednez JC, Kerin S, Suyama J.  (2010)  “Comparison of active cooling devices with passive cooling for rehabilitation of firefighters performing exercise in thermal protective clothing: a report from the Fireground Rehab Evaluation (FIRE) trial”.  Prehospital Emergency Care.  14:300–309.
     
  19. McArdle WD, Mage lJR, Lesmes GR, Pechar GS.  (1976)  “Metabolic and cardiovascular adjustment to work in air and water at 18, 25, and 33 degrees C”.  Journal of Applied Physiology.  40:85–90.
     
  20. Armstrong LE, Crago AE, Adams R, Roberts WO, Maresh CM.  (1996)  “Whole-body cooling of hyperthermic runners:  Comparison of two field therapies”.  American Journal of Emergency Medicine.  14: 355–358.
     
  21. Costrini A.  (1990)  “Emergency treatment of exertional heat stroke and comparison of whole body cooling techniques”.  Medicine & Science in Sports & Exercise.  22:15–18.
     
  22. Casa DJ, McDermott BP, Lee EC, Yeargin SW, Armstrong LE, Maresh CM.  (2007)  “Cold water immersion:  The gold standard for exertional heat stroke treatment”.  Exercise & Sports Sciences Review35:141–149.
     
  23. Kielblock AJ, Van Rensburg JP, Franz RM.  (1986)  “Body cooling as a method for reducing hyperthermia.  An evaluation of techniques”.  South African Medical Journal.  69:378–380.
     
  24. Richards D, Richards R, Schofield PJ, Ross V, Sutton JR. (1979)  “Management of heat exhaustion in Sydney’s the Sun City- to-Surf run runners”.  Medical Journal of Australia.  2:457–461.
     
  25. Downey JA, Darling RC.  (1962)  “Effect of salicylates on elevation of body temperature during exercise”.  Journal of Applied Physiology.  17:323–325.
     
  26. Johnson SC, Ruhling RO.  (1985)  “Aspirin in exercise-induced hyperthermia. Evidence for and against its role”.  Sports Medicine. 2:1–7.