Heat-related illnesses include a spectrum of disorders ranging from heat syncope, muscle cramps, and heat exhaustion to medical emergencies such as heatstroke.
In contrast to severe hyperthermia, the far more common sign of fever reflects intact thermoregulation.
Central thermostat Preoptic nucleus of the Anterior Hypothalamus.
Normally, the body dissipates heat into the environment via four mechanisms. The evaporation of skin moisture is the single most efficient mechanism of heat loss but becomes progressively ineffective as the relative humidity rises to >70%.
The radiation of infrared electromagnetic energy directly into the surrounding environment occurs continuously. Conversely, radiation is a major source of heat gain in hot climates .
Conduction — the direct transfer of heat to a cooler object—and convection —the loss of heat to air currents
Factors that interfere with the evaporation of diaphoresis significantly increase the risk of heat illness. Examples dripping of sweat off the skin constrictive or occlusive clothing, dehydration, and excessive humidity
The regulation of this heat load is complex and involves the central nervous system (CNS), thermosensors , and thermoregulatory effectors. The central thermostat activates the effectors that produce peripheral vasodilation and sweating. The skin surface is in effect the radiator and the principal location of heat loss, since skin blood flow can increase 25–30 times over the basal rate. This dramatic increase in skin blood flow, coupled with the maintenance of peripheral vasodilation, efficiently radiates heat. At the same time, there is a compensatory vasoconstriction of the splanchnic and renal beds.
Acclimatization to heat reflects a constellation of physiologic adaptations that permit the body to lose heat more efficiently. This process often requires one to several weeks of exposure and work in a hot environment .
Heat waves exacerbate the mortality rate, particularly among the elderly and poor and among persons lacking adequate nutrition and access to air-conditioned environments. Exertional heat illness continues to occur when laborers, military personnel, or athletes exercise strenuously in the heat. preadolescents and teenagers are at risk since they may use poor judgment when vigorously exercising in high humidity and heat. Other risk factors include obesity, poor conditioning and lack of acclimatization, and mild dehydration.
Any physiologic or pharmacologic impediment to cutaneous perfusion will impair heat loss.
Calcium channel blockers, beta blockers, and various stimulants also inhibit sweating by reducing peripheral blood flow.
Heat edema is characterized by mild swelling of the hands, feet, and ankles during the first few days of significant heat exposure. The principal mechanism involves cutaneous vasodilation and pooling of interstitial fluid in response to heat stress. resolves without treatment in several days
Prickly heat maculopapular, pruritic, erythematous rash that commonly occurs in clothed areas. Blockage of the sweat pores by debris from macerated stratum corneum causes inflammation in the sweat ducts. As the ducts dilate, they rupture and produce superficial vesicles. The predominant symptom is pruritus. antihistamines, chlorhexidine Clothing should be clean and loose fitting, and activities or environments that induce diaphoresis should be avoided.
Heat syncope exercise-associated collapse Endurance exercise prolonged standing while stationary in the heat Sudden standing after prolonged exposure to heat. relative volume depletion, decreased vasomotor tone, and peripheral vasodilation postural hypotension non-acclimated elderly individuals. removal from the heat source cooling rehydration.
Hyperventilation tetany occurs in some individuals when exposure to heat stimulates hyperventilation, producing respiratory alkalosis, paresthesias , and carpopedal spasm providing reassurance moving the patient out of the heat addressing the hyperventilation.
Heat cramps intermittent, Painful Involuntary spasmodic contractions of skeletal muscles. unacclimated individual who is at rest after vigorous exertion in a humid, hot environment. In contrast, cramps that occur in athletes during exercise last longer, are relieved by stretching and massage, and resolve spontaneously.
replacing fluid losses with copious water or other hypotonic fluids cause Def of NA K rhabdomyolysis Treatment=commercially available electrolyte solutions
Heat exhaustion The physiologic hallmarks of heat exhaustion—in contrast to heatstroke—are the maintenance of thermoregulatory control and CNS function. Laborers, athletes, and elderly individuals exerting themselves in hot environments, without adequate fluid intake, tend to develop water depletion heat exhaustion. In contrast, salt-depletion heat exhaustion occurs more slowly in unacclimated persons who have been consuming large quantities of hypotonic solutions.
diagnosis of exclusion isotonic IV fluids frequent electrolyte determinations
Heat stroke total loss of thermoregulatory function. tachypnea , tachycardias , hypotension, and a widened pulse pressure. physical triad of exposure to a heat stress, CNS dysfunction, and a core temperature >40.5°C helps establish the preliminary diagnosis.
weakness, dizziness, disorientation, ataxia, and gastrointestinal or psychiatric symptoms.
Step 1: Initiate resuscitation • resuscitate and Administer IV fluids promptly as these patients are dehydrated. Step 2: Assess the type of hyperthermia by history and examination • Hyperthermia is a core temperature greater than 104°F.
Step 3: Send investigations Hemogram Creatine phosphokinase—elevated levels suggest hyperthermia. Renal functions Urine for myoglobin When indicated, coagulation studies, toxicologic screening, CT head, and lumbar puncture should be carried out.
Step 4: General management • Ask the patient to rest , preferably in a cool place. • If the patient is conscious, offer fluids but avoid alcohol and caffeine. • Confirm the diagnosis with a calibrated thermometer to measure high temperature (40–47°C). • Encourage him/her to shower and bath, or sponge off with cool water. • There is no role of antipyretics (acetaminophen/acetylsalicylic acid). • Monitor core temperature continuously with a rectal or esophageal probe. • In order to avoid iatrogenic hypothermia, stop cooling at 39.5°C (103°F).
External cooling techniques Conductive cooling- hypothermic blanket, ice bath, or ice packs to neck, axillae, and groins. Avoid vasoconstriction and shivering as vasoconstriction impedes the heat loss and shivering creates heat. Convective techniques include removal of clothing and use of fans and air conditioners. Evaporative cooling can be accelerated by removing clothing and using a fan in conjunction with misting the skin with tepid water or applying a single layer wet sheet to bare skin. Immersing the patient in ice water is the most effective method of rapid cooling but complicates monitoring and access to the patient.
Internal cooling techniques such as ice water gastric or rectal lavage, thoracic lavage, and extracorporeal blood cooling are effective, but they are difficult to manage and are associated with complications. Cold peritoneal lavage results in rapid cooling but is an invasive technique contraindicated in pregnant patients or those with previous abdominal surgery. Cold O2 and cold IV fluids are useful adjuncts
Step 5: Specific management: Malignant hyperthermia and neuroleptic malignant syndrome Dantrolene
Step 6: Manage complications • Rhabdomyolysis – Expand the intravascular volume with normal saline and administer mannitol and sodium bicarbonate. – Alkalinization of urine prevents the precipitation of myoglobin in the renal tubules
Hypotension: To sustain organ perfusion, maintain mean arterial pressure of more than 65 mmHg by fluid administration, consider vasopressors, and monitor central venous pressure. Seizures should be controlled by IV benzodiazepines and barbiturates. Multiorgan failure : Give supportive therapy until organ function recovers.
Step 7: Prevention Hyperthermia, caused by physical exertion or hot environment, can be prevented by taking frequent rest breaks and staying hydrated.
CASE It was the month of MAY; a 55-year-old male laborer became unconscious at work. On examination, he was found to be obtunded with minimal response to painful stimulus. His skin was hot and flushed. He was tachypneic , tachycardiac , hypotensive, and hyperthermic (core temperature 107°F).
• Get the victim out of the sun to a cool place, preferably one that is air-conditioned • Discontinue the presumed causative agent (neuroleptics/ suxamethonium /halothane) • Give IV diazepam 5 mg IV if the patient is having seizures
Assess breathing and pulse
Pulse and breathing present ? O2 inhalation Cold IV fluids Measure core temperature
Pulse or breathing absent ? ACLS CPR PROTOCOL
NEXT 1. Get the victim out of the hot area 2. Loosen the garments 3. Give cold IV saline 4. Give high flow humidified oxygen 5. Do external cooling and avoid vasoconstriction 6. Do internal cooling 7. Treat complications
If cooling is delayed, severe hepatic dysfunction, renal failure, disseminated intravascular coagulation, and fulminant multisystem organ failure may occur. Hepatocytes are very heat sensitive