Exertional Heatstroke

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.