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The (not so) New Hotness: Heat Illness & EMS

by Curbside to Bedside

Intro

  • Heat Stroke is broadly defined as a core temperature above 104 F with central nervous system abnormalities following strenuous exercise or environmental heat. – Wilderness Medical Society.
  • Heat cramps, exhaustion, illness, stroke etc. are a spectrum of a single illness (systemic non drug related hyperthermia) rather than each being an individual entity.

  • THE CARDINAL SIGN OF HEAT STROKE IS ALTERED MENTAL STATUS

    • Anhydrosis is not a reliable finding, and should not be used as a clinical guidepost.

Pathophysiology

  • An increase in blood temp triggers hypothalamic thermoregulation it increase blood flow to the skin – cutaneous vasodilation – blood shunts the the periphery to facilitate heat loss through sweating.
  • Renal and splanchnic perfusion is reduced.
  • Heat stroke produces an inflammatory response similar to that seen in sepsis.
  • Increased mucosal permeability from inflammatory mediators allows endotoxins from the gut to enter systemic circulation – leading to alterations in microcirculation, more endothelial and tissue injury, and impaired thermoregulation.

Prevention and Acclimatization

  • Acclimatization may be likened to receiving a “heat vaccine” with small steady doses of exertion in hot environments provoking an adaptive response within the body.
  • 1-2 hours of progressive, controlled, heat-exposed exertion per day for 10-14 days.
  • This adaptation may persist up to a month.
  • One bout of a heat stroke may reset thermoregulatory adaptations and increase risk for subsequent heat injury for months.
  • Hyperhydration has no effect on heat tolerance.
  • Forced hydration is ineffective and dangerous (hyponatremia risk).

Environmental Considerations

  • Wet Bulb Globe Temperature
    • “Composite” temperature factoring humidity, sun angle, apparent temperature, wind speed, and solar radiation.
    • Generally considered more accurate than the Heat Index, which is a function of temperature and humidity in shaded areas.
  • As the environmental temperature increases the body will incur a net heat gain through convective and radiative processes, leaving evaporative thermoregulation as the only cooling mechanism.
  • Some activities enhance heat transfer: Cyclist, swimmers, etc.
  • Increased metabolic demand and increased ambient conditions should lead to breaks in proportion to both.

Field Treatment Principles

  • Rapid, often empiric, cold water immersion is the gold standard treatment.
  • Rapid reversal of the condition is key: morbidity and mortality is directly associated with the duration of hyperthermia experienced by the patient.
  • If a patient is hyperthermic and has AMS, empiric cooling should not be delayed to obtain a temperature – or if temperature is less than 104 F, it should not deter you from aggressive cooling measures.
  • Naturally, manage ABCs as needed.
  • Treatment on scene is preferred over rapid transport.

Cold Water Immersion Therapy

  • CWIT is the gold standard of treatment, and usually involves placing a patient’s entire body (with airway protection measures in place) in a tub or trough of cold water.
  • CWIT is two times more effective in heat transfer than spraying cool water over the body.
  • Hindrance of cooling in the setting of EHS due to shivering has been physiologically refuted.

Other Cooling Methods

  • If CWIT is not available, repeated dousing of cold water over the patient is “next best”.
  • Ice Sheets placed over the patient’s body and exchanged every 2-3 minutes is an approach often adapted by the military where carrying large troughs of ice water is not optimal.
  • Axillary or inguinal placement of chemical cold packs or ice is not effective.
  • Be creative! The goal is to get large volumes of water over the patient or place the patient in a body of water to maximize the effect of convective cooling.

Temperature Monitoring

  • Rectal and/or esophageal temperature monitoring is the gold standard.
  • Oral, axillary, or skin temperature readings are highly likely to be inaccurate.
  • Temperature monitoring is not required to initiate therapy, but may be helpful to guide therapy or consider other differential diagnoses.

Now for the Podcast:

References

 

TB MED 507: Heat Stress Control and Heat Casualty Management
https://www.dir.ca.gov/OSHSB/documents/Heat_illness_prevention_tbmed507.pdf

TC 4-02.3: Field Hygiene and Sanitation
https://armypubs.army.mil/epubs/DR_pubs/DR_a/pdf/web/tc4_02x3.pdf

FM 4-02.17: Preventative Health Services
https://www.google.com/search?q=fm+4-02.17&ie=utf-8&oe=utf-8&client=firefox-b-1-ab

TRADOC 350-29: Prevention of Heat and Cold Casualties
http://www.tradoc.army.mil/tpubs/regs/tr350-29.pdf

 Lipman, G. S., Eifling, K. P., Ellis, M. A., Gaudio, F. G., Otten, E. M., & Grissom, C. K. (2014). Wilderness medical society practice guidelines for the prevention and treatment of heat-related illness: 2014 update. Wilderness and Environmental Medicine. https://doi.org/10.1016/j.wem.2014.07.017

Sawka, M. N., Leon, L. R., Montain, S. J., & Sonna, L. A. (2011). Integrated physiological mechanisms of exercise performance, adaptation, and maladaptation to heat stress. Comprehensive Physiology, 1(4), 1883–1928. https://doi.org/10.1002/cphy.c100082

Carter, R., Cheuvront, S. N., Williams, J. O., Kolka, M. A., Stephenson, L. A., Sawka, M. N., & Amoroso, P. J. (2005). Epidemiology of hospitalizations and deaths from heat illness in soldiers. Medicine and Science in Sports and Exercise, 37(8), 1338–1344. https://doi.org/10.1249/01.mss.0000174895.19639.ed

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APHC Fact Sheet
https://phc.amedd.army.mil/PHC%20Resource%20Library/HeatIllness_FS_12-005-0316.pdf

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