A. Introduction

1. Definition of Heat Stress
   1. Perceived discomfort and physiologic stress
   2. Associated with exposure to hot environment
   3. Especially during physical work
   4. Sunburn, especially severe, can precipitate event
2. Definition of Heat Stroke
   1. Body temperature >40°C (104°F)
   2. Central nervous sytem (CNS) anomalies: delirium, convulsions, or coma
   3. Hot, dry skin (indicates dehydration)
   4. Humidity is a major contributor
   5. Classified as exertional or classic
3. Classic Heat Stroke
   1. Typically reported in elderly persons during heat waves [2,3]
   2. No sweating (anhidrosis)
   3. Social isolation and lack of air conditioning are risk factors [2]
   4. Some reports that acute renal failure and rhabdomyolysis are uncommon [2]
   5. However, multiorgan-system failure (MOSF) similar to that in exertional heat stroke [3]
   6. Neurologic symptoms and disseminated intravascular coagulation (DIC) occur as well
   7. Increased Risk: heart failure, diabetes, EtOH intoxication, severe scleroderma
4. Exertional Heat Stroke
   1. Young People
   2. Sporadic
   3. Normal sweat response, usually in setting of heavy exertion
   4. Common: Rhabdomyolysis, Lactic Acidosis, Renal Failure
   5. Severe: MOSF, DIC, obtundation

B. Pathophysiology [1]

1. Thermoregulation
   1. Heat gained from environment and produced by metabolism
   2. Heat is dissipated to maintain body temperature of 37°C (98.6°F)
   3. Rise in blood temperature activates peripheral and hypothelamic heat receptors
   4. These signal hypothalamic thermoregulatory center
   5. Stimulates sympathetic outflow with cutaneous vasodilation
   6. Blood flow to skin increases by up to 8 liters per minute
   7. Splanchnic vasoconstriction accompanies increased flow to skin
   8. Sweat will also evaporate if ambient humidity is not over ~90%
   9. Sweating can dissipate up to 600 kcal/hour
   10. This may lead to dehydration and salt loss, compromising renal function
2. Acute Phase Response to Heat Stress
   1. Endothelium, epithelium and leukocytes primarily involved
   2. Response to heat ledas to cytokine induction
   3. Interleukin (IL) 1ß, IL6, tumor necrosis factor alpha (TNFa) are major mediators
   4. Many other cytokines play key roles
   5. IL6 stimulates acute phase reactant production by liver
   6. Inflammatory cytokines may increase bacterial endotoxin leakage through the gut
   7. Increased levels of circulating endotoxin may be seen in heat stress and shock
   8. Heat shock is an exaggeration of the acute-phase response
3. Vasodilation
   1. Elevated levels of inflammatory and anti-inflammatory cytokines active endothelium
   2. Endothelial activation leads to elevated nitric oxide production
   3. Nitric oxide causes vasodilation
   4. Vasodilation with dehydration and salt loss can lead to hypotension
   5. Hypoperfusion of organs due to hypotension and blood shunting occurs
   6. Organ dysfunction can occur, and may progress to MOSF
4. Organ Dysfunction
   1. Respiratory Failure - pulmonary edema
   2. Seizures
   3. Renal Failure - prerenal, rhabdomyolysis (myoglobulinuria)
   4. Shock liver can also occur

C. Signs an Symptoms [1,3]

1. Loss of consciousness may be presenting symptom
2. Neurologic Symptoms are prominant
   1. Headache, Vertigo, Faintness
   2. Confusion or Delirium
   3. Seizures
   4. Coma
   5. Stroke (Focal Deficit)
3. Abdominal Distress
4. Body Temperature >40.5°C; temperatures >41°C (106°F) are common
   1. Pyrexia
   2. Prostration
5. Skin
   1. Hot and Dry in classic heat stroke
   2. Wet, normal sweat response in exertional
   3. Evidence of (severe) sunburn may be present
6. Tachypnea is common
7. Rapid pulse usually with reduced blood pressure
8. Flaccid muscles, decreased deep tendon reflexes
9. Frank heart failure may be present

D. Laboratory

1. Leukocytosis - stress response
2. Hemoconcentration - dehydration
3. Early Renal Findings
   1. Proteinuria
   2. BUN elevation - probably due to increased tissue destruction at high temperatures
   3. BUN also elevated with dehydration
   4. Renal insufficiency is very common; may progress to renal failure
4. Mixed Acid-Base Disorder
   1. Respiratory Alkalosis - heat exchange through respiration
   2. Metabolic Acidosis - lactic acidosis
5. Renal Failure
   1. Myoglobulinuria apears to be major contributor
   2. Oliguria or anuria can occur
   3. Evaluate for acute tubular necrosis
6. DIC may occur
   1. Disseminated intravascular coagulopathy (DIC)
   2. Petechiae, purpura, hematemesis, epistaxis
   3. PT and APTT prolonged, platelet count near normal
   4. Fibrin degradation products (FDPs) elevated
   5. D-Dimers present
7. Liver damage can occur 24-36 hours post-admission
8. Full Multiple Organ-System Failure (MODS) may ensue
   1. Renal Insufficiency / Failure
   2. DIC
   3. Acute respiratory distress syndrome
   4. Suppression of left ventricular cardiac function

E. Differential of Very High Fever

1. Malignant Hyperthermia
2. Neuroleptic Malignant Syndrome
3. Severe Hyperthyroidism
4. Meningitis (sepsis occasionally gives very high fevers)
5. Rocky Mountain Spotted Fever
6. Drug Reaction
7. Cerebral Malaria
8. Heat Stroke
9. Still's Disease

F. Therapy

1. Remove all clothing
2. Immediate shower, lukewarm water recommended
3. Fan (cool air) to dissipate heat
4. Lower rectal temperature to 100-102°F within 30-60 minutes
   1. Ice bath not effective
   2. Good fluid resuscitation - usually intravenously, with cooling
   3. May need Central Venous access (particularly for intensive monitoring)
5. Monitoring for electrolyte imbalances
   1. Full serum electrolytes
   2. Including calcium, magnesium, phosphorus
6. Arrhythmia Monitoring
7. Toxicology screen may be helpful to determine medications, underlying conditions
8. Pulmonary Artery Measurements may be helpful with cardiovascular dysfunction
9. Search for evidence of infection [3]
10. Avoid large doses of tylenol and NSAIDs

Resources

Celsius ==> Fahrenheit

References

1. Bouchama A and Knochel JP. 2002. NEJM. 346(25):1978
2. Semenza JC, Rubin CH, Falter KH, et al. 1996. NEJM. 335(2):84
3. Dematte JE, O'Mara K, Buescher J, et al. 1998. Ann Intern Med. 129(3):173