Heat Exhaustion

HEAT EXHAUSTION

PATHOPHYSIOLOGY

Heat exhaustion is a syndrome of volume depletion secondary to heat stress. Most often, heat exhaustion manifests as physical collapse during exercise. Heat exhaustion is subdivided by etiology of volume loss into water depletion and salt depletion subgroups (Platt, 2014). Heat exhaustion is a form of major heat illness, along the same spectrum of disease as heat stroke. It is important to note that both types heat exhaustion will progress to heat stroke if left untreated.

Water depletion heat exhaustion is the result of net fluid loss in the setting of environmental heat stress. Both athletes and non-athletes will rarely replace all the water they lose through sweating while under environmental heat stress. Progressively, this volume depletion will eventually reach the point of cardiovascular compromise and if left untreated may progress to hypovolemic shock as water loss continues (Toru Hifumi, 2018).

Sweat contains 0.9 grams of sodium per litre (Joshua, 2015). Thus, as individuals sweat, they progressively become sodium deplete. Given that significant volumes of water are also lost through sweating, the concentration of sodium remains within homeostatic ranges as salt and water losses are proportional. If the volume of fluid loss through sweating is replaced with hypotonic fluid of low salt concentration such as free water, then sodium concentrations may plummet abruptly through dilution (Platt, 2014). This is the basis for salt depletion heat exhaustion. Typically, salt depletion will require longer to develop than water depletion. However, the sequala of cardiovascular compromise and eventual hypovolemic shock is the same for both subtypes (Joshua, 2015).

Pure forms of either type of heat exhaustion are rare. More commonly, individuals will have a combination of both water and salt depletion. Common risk factors for the development of either subtype of heat exhaustion include:

• Poor access to drinking water
• Prolonged exertion > 4 hours
• Poor mobility
• Dementia
• Diabetes
• Renal impairment
• Lack of acclimatization
• High sweat salt concentration
• Ingesting large volumes of hypotonic fluid
• Thiazide diuretics

CLINICAL PRESENTATION & DIAGNOSIS

The clinical features of both water and salt depletion heat exhaustion are similar. Symptoms tend to be variable and non-specific, particularly early on in the disease course. Physical collapse, malaise, fatigue, headache, palpitations, nausea, vomiting, impaired judgement, and muscle cramps are commonly reported symptoms. Examination typically reveals, sinus tachycardia, tachypnea, flushed skin, and profuse sweating. Orthostatic dizziness and syncope suggest a greater degree of volume contraction, especially in athletes. Core temperatures are often normal, if not slightly elevated. Core temperatures should never exceed 40°C. There should be no signs of central nervous system dysfunction and mental status should be normal. If any alteration in mental status is present the patient should be treated as having heat stroke (Platt, 2014).

DIFFERENTIAL

• Heat stroke
• Hyponatremia
• Infection
• Thyroid storm
• Encephalitis
• Sympathomimetic ingestion
• Serotonin syndrome
• Seizure

TREATMENT

Regardless of subgroup, patients with suspected heat exhaustion should be removed from play and placed in a shaded or air-conditioned area. All excessive clothing and equipment should be removed to maximize evaporative cooling. Patient with heat exhaustion have intact thermoregulatory mechanisms, they do not require active cooling as a life saving measure the way heat stroke patients do (Platt, 2014).

Cooling in the setting of heat exhaustion is primarily for patient comfort and may be performed using cold oral fluids and ice packs around the neck, axilla, and groin. If cooling is utilized, a core temperature target of 38°C should be used to prevent overshoot and subsequent hypothermia. Heat exhaustion patients should be orally rehydrated with isotonic electrolyte solutions such as sports drinks. If unable to tolerate oral intake transport to hospital for intra-venous fluid repletion may be required. If any neurologic dysfunction becomes apparent, the patient should be presumed to have heat stroke and treated accordingly (Platt, 2014).

Authors Dr. Erik Leci and Dr. Graham Briscoe (May 10, 2020 PR ND)

References:

Platt, a. P. (2014). Heat Illness . In H. W. Marx, Rosen’s emergency medicine: Concepts and clinical practice (8th ed.) (pp. 1896 – 1905). Philadelphia, PA: Elsevier/Saunders. .

Toru Hifumi, Y. K. (2018). Heat stroke. Journal of Intensive Care , 320-328.

Joshua, D. G. (2015). Adaptation to Hot Environmental Conditions: An Exploration of the Performance Basis, Procedures and Future Directions to Optimise Opportunities for Elite Athletes. Sports Medicine, 303 -311.