Heat Stroke Summary
Research Summary
Hunter Jones
MICT III Clinical
Johnson County Community College
Research Summary
Heat stroke is defined by Knochel and Ouchama (2002, p. 1978) as “a core body temperature that rises above 40°C (105°F) and that is accompanied by hot, dry skin and central nervous system abnormalities such as delirium, convulsions, or coma.” Heat stroke can be the result of either exposure to a high environmental temperature or from an elevated core temperature due to strenuous exercise. However, due to the presentation of an ‘unconscious unknown’ the diagnosis of heat stroke can be a difficult one. Sudden loss of consciousness is a common presenting complaint in emergency departments. The complaint is evidence of a wide …show more content…
disease spectrum. Additionally, this patient group has a high mortality rate: 31.3% according to one study. Also according the same study by McLaren, Lear, and Daniels (1994, p. 138) “these deaths occurred largely in the elderly and it is suggested that elderly patients should either be admitted for observation, or a careful screening carried out for underlying pathology.” In light of this information, it is imperative that healthcare providers consider all causes of AMS (altered mental status), including heat stroke.
Disease or injury pathophysiology
The pathogenesis of heat stroke can best be understood by looking at it in three distinct phases of cellular response to heat stress: thermoregulation, an acute-phase response, and a response that involves the production of ‘heat-shock’ proteins. A dysfunction in any of these phases can result in heat stroke.
Body heat is both gained from the external environment and produced in the body through metabolism. Knochel et. al (2002, p. 1980) states, “heat load must be dissipated to maintain a body temperature of 37°C, a process called thermoregulation. A rise in the temperature of the blood by less than 1°C activates peripheral and hypothalamic heat receptors that signal the hypothalamic thermoregulatory center, and the efferent response from this center increases the delivery of heated blood to the surface of the body.” When this pathway is overexerted it can lead to dysfunction and increase the likelihood of heat stroke. Also, damage to the hypothalamus through stress can lead to a permanent inability to regulate internal temperature.
Knochel et. al. (2002, 1981) further states, “the acute-phase response to heat stress is a coordinated reaction that involves endothelial cells, leukocytes, and epithelial cells and that protects against tissue injury and promotes repair.” Chemical mediators of inflammation include Interleukin-1 and a variety of other cytokines. Of these, Interleukin-1 was the first known mediator induced by strenuous exercise. These chemical mediators control systemic PVR (peripheral vascular resistance). If this pathway is exaggerated, it can lead to the distributive shock seen in heat stroke.
Cells respond to a sudden increase in heat by producing proteins. These proteins are known as heat-shock proteins. Their expression is controlled in the cell at the level of the genes. Knochel et. al. (2002, p. 1981) also states, “during stress, one or more heat-shock transcription factors bind to the heat-shock element, resulting in an increased rate of transcription of heat-shock proteins. Increased levels of heat-shock proteins in a cell induce a transient state of tolerance to a second, otherwise lethal, stage of heat stress, allowing the cell to survive.” Again, if this pathway is overexerted, stressed through an intolerable heat exposure, it will lead to the permanent dysfunction of the thermoregulatory center, circulatory collapse, and renal failure.
Demographics, etiology, incidence, morbidity/mortality
All people are susceptible to the development of heat stroke. However, there is considerable variation among populations. Specifically, elderly patients have a lower threshold for the development of the complications of heat stroke. This occurs for a number of reasons. First, elderly patients are often placed in low sodium diets in order to treat hypertension. This predisposes elderly patients to the development of dehydration, and in turn, this dehydration decreases heat tolerance. Second, as Flynn, McGreevy, and Mulkerrin (2005, p. 227) note, “an age-related decline in plasma renin and aldosterone levels predisposes to natriuresis, diuresis and salt depletion in older patients, even when they are water- and salt-deprived. Total body water decreases with increasing age, and this is associated with an increase in fat and a decrease in lean body mass.” Elderly patients have less bodily reserve and therefore produce lower levels of heat-shock proteins and are more sensitive to inflammatory mediators.
During ‘heat-waves’ the majority of deaths occur within the elderly population. A study in France conducted by Flynn et. al. (2005, p. 227) revealed, “more than 11 000 people were registered as dying in France during the first two weeks of August in 2003. The majority of excess mortality appears to have occurred in older, frail individuals who were thought to have tolerated poorly the extremes of heat experienced in France at that time.”
Classic signs/symptoms; atypical presentations
There are two findings required for the diagnosis of heat stroke: hyperthermia and central nervous system dysfunction. Hyperthermia may range anywhere from 40°C to 47°C. Brain dysfunction is typically severe but it may also be subtle. Deficits may manifest only as impaired judgment. Knochel et al (2002, p. 1983) states “seizures may occur, especially during cooling. All patients have tachycardia and hyperventilation. In either classic or exertional heat stroke, the arterial carbon dioxide tension is often less than 20 mm Hg. Twenty-five percent of patients have hypotension. Patients with non-exertional heat stroke usually have respiratory alkalosis.” However, it is interesting to note that those patients with exertional heat stroke usually have both respiratory alkalosis and lactic acidosis. Knochel et al (2002, p. 1983) further states, “hypophosphatemia and hypokalemia are common at the time of admission. Hypoglycemia is rare. Hypercalcemia and hyperproteinemia, reflecting hemoconcentration, may also occur. In patients with exertional heat stroke, rhabdomyolysis, hyperphosphatemia, hypocalcemia, and hyperkalemia may be important events after complete cooling.” The most serious complication of heat stroke is MODS (multiorgan-dysfunction syndrome). Symptoms of MODS include encephalopathy, rhabdomyolysis, acute renal failure, acute respiratory distress, myocardial injury, liver injury, pancreatic injury, and hemorrhage.
Typical clinical course, typical treatment, clinical significance, prognosis
The most effective treatment is the removal of the patient from the environment and cooling.
Knochel et al (2002, p. 1986) states, “effective heat dissipation depends on the rapid transfer of heat from the core to the skin and from the skin to the external environment. In persons with hyperthermia, transfer of heat from the core to the skin is facilitated by active cutaneous vasodilatation. Therapeutic cooling techniques are therefore aimed at accelerating the transfer of heat from the skin to the environment without compromising the flow of blood to the skin. This is accomplished by increasing the temperature gradient between the skin and the environment.” It is common practice today to use cold water or ice on the skin. However, these methods lower the skin temperature to a point that may trigger vasoconstriction and shivering. Knochel et al (2002, p. 1986) say that “to overcome this response, the patient may be vigorously massaged, sprayed with tepid water (40°C), or exposed to hot moving air (45°C), either at the same time as cooling methods are applied or in an alternating fashion.” There are currently no pharmacologic agents that are able to accelerate cooling in the treatment of heat stroke. However, dantrolene sodium has been considered. The goal of treatment should be the recovery of central nervous system function. A review study conducted by Vicario, Okabajue, and Haltom (1986, p. 395) record “the case of 39 patients with classic (non-exertional) heat stroke presenting to an urban emergency department were reviewed. Eight of 39 patients died. Rapid cooling, defined as a rectal temperature of ≤38.9°C (102°F) within an hour of presentation, was achieved in 27 of 39 patients. Twelve patients had a temperature ≥38.9°C (102°F) after one hour of treatment in the emergency department. The rate of mortality in the rapid cooling group was four of 27 (15%), while in the delayed cooling group, the mortality rate was four of 12 (33%) (P = 0.18).” This review study
suggests that rapid cooling to 102°F is the most effective way to lower mortality in non-exertional heatstroke. However, the authors also stated that factors such as age, hypotension, and the necessity for intubation on presentation all predisposed to a higher mortality rate despite effective cooling.
References
Flynn, A, and C. McGreevy, and E. Mulkerrin. (2005). Why Do Older Patients Die in a Heat
Wave?. Q J Med, 98 pp. 227-229.
McLaren, A. J, and J. Lear, and R. Daniels. (1994). Collapse in an Accident and Emergency
Department. Journal of the Royal Society of Medicine, 87 pp. 138-139.
Ouchama, A. B, and J. Knochel. (2002). Heat Stroke. New England Journal of Medicine, 346
(25), pp. 1978-1988.
Schuman, S. H. (1972). Patterns of urban heat-wave deaths and implications for prevention: Data from New York and St. Louis during July, 1966. Environmental Research, 5 (1), pp. 59-75.
Vicario, S. J, and R. Okabajue, and T. Haltom. (1986). Rapid cooling in classic heatstroke: Effect on mortality rates. The American Journal of Emergency Medicine, 4 (5), pp. 394-398
Hunter Jones
MICT III Clinical
Johnson County Community College
Research Summary
Heat stroke is defined by Knochel and Ouchama (2002, p. 1978) as “a core body temperature that rises above 40°C (105°F) and that is accompanied by hot, dry skin and central nervous system abnormalities such as delirium, convulsions, or coma.” Heat stroke can be the result of either exposure to a high environmental temperature or from an elevated core temperature due to strenuous exercise. However, due to the presentation of an ‘unconscious unknown’ the diagnosis of heat stroke can be a difficult one. Sudden loss of consciousness is a common presenting complaint in emergency departments. The complaint is evidence of a wide …show more content…
disease spectrum. Additionally, this patient group has a high mortality rate: 31.3% according to one study. Also according the same study by McLaren, Lear, and Daniels (1994, p. 138) “these deaths occurred largely in the elderly and it is suggested that elderly patients should either be admitted for observation, or a careful screening carried out for underlying pathology.” In light of this information, it is imperative that healthcare providers consider all causes of AMS (altered mental status), including heat stroke.
Disease or injury pathophysiology
The pathogenesis of heat stroke can best be understood by looking at it in three distinct phases of cellular response to heat stress: thermoregulation, an acute-phase response, and a response that involves the production of ‘heat-shock’ proteins. A dysfunction in any of these phases can result in heat stroke.
Body heat is both gained from the external environment and produced in the body through metabolism. Knochel et. al (2002, p. 1980) states, “heat load must be dissipated to maintain a body temperature of 37°C, a process called thermoregulation. A rise in the temperature of the blood by less than 1°C activates peripheral and hypothalamic heat receptors that signal the hypothalamic thermoregulatory center, and the efferent response from this center increases the delivery of heated blood to the surface of the body.” When this pathway is overexerted it can lead to dysfunction and increase the likelihood of heat stroke. Also, damage to the hypothalamus through stress can lead to a permanent inability to regulate internal temperature.
Knochel et. al. (2002, 1981) further states, “the acute-phase response to heat stress is a coordinated reaction that involves endothelial cells, leukocytes, and epithelial cells and that protects against tissue injury and promotes repair.” Chemical mediators of inflammation include Interleukin-1 and a variety of other cytokines. Of these, Interleukin-1 was the first known mediator induced by strenuous exercise. These chemical mediators control systemic PVR (peripheral vascular resistance). If this pathway is exaggerated, it can lead to the distributive shock seen in heat stroke.
Cells respond to a sudden increase in heat by producing proteins. These proteins are known as heat-shock proteins. Their expression is controlled in the cell at the level of the genes. Knochel et. al. (2002, p. 1981) also states, “during stress, one or more heat-shock transcription factors bind to the heat-shock element, resulting in an increased rate of transcription of heat-shock proteins. Increased levels of heat-shock proteins in a cell induce a transient state of tolerance to a second, otherwise lethal, stage of heat stress, allowing the cell to survive.” Again, if this pathway is overexerted, stressed through an intolerable heat exposure, it will lead to the permanent dysfunction of the thermoregulatory center, circulatory collapse, and renal failure.
Demographics, etiology, incidence, morbidity/mortality
All people are susceptible to the development of heat stroke. However, there is considerable variation among populations. Specifically, elderly patients have a lower threshold for the development of the complications of heat stroke. This occurs for a number of reasons. First, elderly patients are often placed in low sodium diets in order to treat hypertension. This predisposes elderly patients to the development of dehydration, and in turn, this dehydration decreases heat tolerance. Second, as Flynn, McGreevy, and Mulkerrin (2005, p. 227) note, “an age-related decline in plasma renin and aldosterone levels predisposes to natriuresis, diuresis and salt depletion in older patients, even when they are water- and salt-deprived. Total body water decreases with increasing age, and this is associated with an increase in fat and a decrease in lean body mass.” Elderly patients have less bodily reserve and therefore produce lower levels of heat-shock proteins and are more sensitive to inflammatory mediators.
During ‘heat-waves’ the majority of deaths occur within the elderly population. A study in France conducted by Flynn et. al. (2005, p. 227) revealed, “more than 11 000 people were registered as dying in France during the first two weeks of August in 2003. The majority of excess mortality appears to have occurred in older, frail individuals who were thought to have tolerated poorly the extremes of heat experienced in France at that time.”
Classic signs/symptoms; atypical presentations
There are two findings required for the diagnosis of heat stroke: hyperthermia and central nervous system dysfunction. Hyperthermia may range anywhere from 40°C to 47°C. Brain dysfunction is typically severe but it may also be subtle. Deficits may manifest only as impaired judgment. Knochel et al (2002, p. 1983) states “seizures may occur, especially during cooling. All patients have tachycardia and hyperventilation. In either classic or exertional heat stroke, the arterial carbon dioxide tension is often less than 20 mm Hg. Twenty-five percent of patients have hypotension. Patients with non-exertional heat stroke usually have respiratory alkalosis.” However, it is interesting to note that those patients with exertional heat stroke usually have both respiratory alkalosis and lactic acidosis. Knochel et al (2002, p. 1983) further states, “hypophosphatemia and hypokalemia are common at the time of admission. Hypoglycemia is rare. Hypercalcemia and hyperproteinemia, reflecting hemoconcentration, may also occur. In patients with exertional heat stroke, rhabdomyolysis, hyperphosphatemia, hypocalcemia, and hyperkalemia may be important events after complete cooling.” The most serious complication of heat stroke is MODS (multiorgan-dysfunction syndrome). Symptoms of MODS include encephalopathy, rhabdomyolysis, acute renal failure, acute respiratory distress, myocardial injury, liver injury, pancreatic injury, and hemorrhage.
Typical clinical course, typical treatment, clinical significance, prognosis
The most effective treatment is the removal of the patient from the environment and cooling.
Knochel et al (2002, p. 1986) states, “effective heat dissipation depends on the rapid transfer of heat from the core to the skin and from the skin to the external environment. In persons with hyperthermia, transfer of heat from the core to the skin is facilitated by active cutaneous vasodilatation. Therapeutic cooling techniques are therefore aimed at accelerating the transfer of heat from the skin to the environment without compromising the flow of blood to the skin. This is accomplished by increasing the temperature gradient between the skin and the environment.” It is common practice today to use cold water or ice on the skin. However, these methods lower the skin temperature to a point that may trigger vasoconstriction and shivering. Knochel et al (2002, p. 1986) say that “to overcome this response, the patient may be vigorously massaged, sprayed with tepid water (40°C), or exposed to hot moving air (45°C), either at the same time as cooling methods are applied or in an alternating fashion.” There are currently no pharmacologic agents that are able to accelerate cooling in the treatment of heat stroke. However, dantrolene sodium has been considered. The goal of treatment should be the recovery of central nervous system function. A review study conducted by Vicario, Okabajue, and Haltom (1986, p. 395) record “the case of 39 patients with classic (non-exertional) heat stroke presenting to an urban emergency department were reviewed. Eight of 39 patients died. Rapid cooling, defined as a rectal temperature of ≤38.9°C (102°F) within an hour of presentation, was achieved in 27 of 39 patients. Twelve patients had a temperature ≥38.9°C (102°F) after one hour of treatment in the emergency department. The rate of mortality in the rapid cooling group was four of 27 (15%), while in the delayed cooling group, the mortality rate was four of 12 (33%) (P = 0.18).” This review study
suggests that rapid cooling to 102°F is the most effective way to lower mortality in non-exertional heatstroke. However, the authors also stated that factors such as age, hypotension, and the necessity for intubation on presentation all predisposed to a higher mortality rate despite effective cooling.
References
Flynn, A, and C. McGreevy, and E. Mulkerrin. (2005). Why Do Older Patients Die in a Heat
Wave?. Q J Med, 98 pp. 227-229.
McLaren, A. J, and J. Lear, and R. Daniels. (1994). Collapse in an Accident and Emergency
Department. Journal of the Royal Society of Medicine, 87 pp. 138-139.
Ouchama, A. B, and J. Knochel. (2002). Heat Stroke. New England Journal of Medicine, 346
(25), pp. 1978-1988.
Schuman, S. H. (1972). Patterns of urban heat-wave deaths and implications for prevention: Data from New York and St. Louis during July, 1966. Environmental Research, 5 (1), pp. 59-75.
Vicario, S. J, and R. Okabajue, and T. Haltom. (1986). Rapid cooling in classic heatstroke: Effect on mortality rates. The American Journal of Emergency Medicine, 4 (5), pp. 394-398