Materiały źródłowe

• #1 Heat Stroke: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/166320-overview

  Heat illness may be viewed as a continuum of illnesses relating to the body’s inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, heat tetany, as well as heat syncope and heat exhaustion. Heat stroke is the most severe heat-related illness and is defined as a body temperature higher than 40C (104F) associated with neurologic dysfunction. […] Heat stroke is defined as hyperthermia exceeding 40C (104F) associated with an altered sensorium. […] Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, potentially leading to heat stroke. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death.

• #2 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  Heatstroke is a severe heat-related illness involving an elevation in body temperature, typically but not always greater than 40 C. The patient has clinical signs of central nervous system dysfunction that may include confusion, ataxia, delirium, or seizures brought on after strenuous physical exertion or exposure to hot weather. […] Heat-related illness is a spectrum of conditions progressing from heat exhaustion and heat injury to life-threatening heat stroke. Heat stroke is a clinical constellation of symptoms that include a severe elevation in body temperature, typically, but not always, greater than 40C. Also, there must be clinical signs of central nervous system dysfunction, including ataxia, delirium, or seizures, in the setting of exposure to hot weather or strenuous physical exertion.

• #3 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health

  https://msdh.ms.gov/page/43,3942,98,261.html

  Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.

• #4 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.

• #5 Heat stroke in children – UpToDate

  https://www.uptodate.com/contents/heat-stroke-in-children

  As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation to allow for reduction of body heat. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. Above 42°C (108°F), oxidative phosphorylation becomes uncoupled and a variety of enzymes cease to function. […] These pathophysiologic changes result in a systemic inflammatory response that causes multiple organ dysfunction and injury. […] The critical thermal maximum (CTM) is defined as the degree of elevated body temperature and duration of heat exposure that can be tolerated before cell damage occurs. […] Physiologic heat stress causes cell injury through several proposed mechanisms: Production of acute-phase reactants (eg, cytokines) that initiate an inflammatory cascade; Direct injury to cells with denaturation of proteins; Direct injury to the vascular endothelium resulting in impaired microcirculation and disseminated intravascular coagulation; Intestinal ischemia and increased permeability followed by endotoxemia.

• #6 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  A person’s ability to thermoregulate is closely linked to the ability of the cardiovascular system to cope with central and peripheral blood flow demands to support metabolic and thermoregulatory requirements. […] Effective thermoregulatory pathways must be active to provide means for heat loss to prevent EHS during severe or prolonged physical activity. […] A thermoregulatory failure underlying EHS would signify a suppressed ability to dissipate heat coupled with high rates of heat storage, which would result in a marked elevation in core temperature. […] Increased intestinal permeability, also known as the leaky gut hypothesis, suggests that bacteria and toxins leak from the gut lumen, where they are normally contained via tight junctions, through the intestinal wall into the portal and general circulation.

• #7 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  It is important to differentiate where the patient is on the heat illness continuum. The signs and symptoms of heat exhaustion may present similarly, including cramping, fatigue, dizziness, nausea, vomiting, and headache. If progression to end-organ damage occurs, it then becomes heat injury. Finally, neurologic alteration distinguishes heat stroke from heat injury. […] Normally, thermoregulation is an extremely efficient process, with a mere 1C change in core temperature for every 25C to 30C change in ambient temperature. In the adapted state, heat-shock proteins repair the damage caused by hyperthermia. The body’s ability to dissipate heat through increased cardiac output, vasoconstriction of splanchnic circulation, and sweating maintain the effective temperature range of these proteins. However, evaporative cooling becomes ineffective if environmental humidity is above 75%.

• #8 Pediatric heat stroke: The danger of children left in hot cars | Pediatric Emergency Medicine

  https://www.acep.org/pediatrics/education/education-articles/heat-stroke-article

  Heat stroke occurs when the bodys thermoregulatory mechanisms are overwhelmed, leading to an increase in core body temperature. […] The principal mechanism of heat loss in a hot environment is evaporation. However, this becomes ineffective above a relative humidity of 75%. […] Children with heat stroke require aggressive treatment because the extent of end-organ damage and mortality is related to the duration of hyperthermia. […] Heat stroke in children left in hot cars is a preventable tragedy that requires vigilance and proactive measures.

• #9 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health

  https://msdh.ms.gov/page/43,3942,98,261.html

  Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.

• #10 Heatstroke – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/heat-stroke/symptoms-causes/syc-20353581

  Heatstroke is a condition caused by the body overheating. This usually happens because of exposure to high temperatures or physical activity in high temperatures for too long. There are a few stages of heat injury, and heatstroke is the most serious. It can happen if body temperature rises to 104 F (40 C) or higher. Heatstroke needs emergency care. If it’s not treated, heatstroke can quickly damage the brain, heart, kidneys and muscles. This damage gets worse the longer treatment is delayed, which increases the risk of serious complications or death. […] Heatstroke can happen as a result of: Being in a hot environment. In a type of heatstroke, called nonexertional (classic) heatstroke, being in a hot environment leads to a rise in core body temperature. This type of heatstroke typically happens after exposure to hot, humid weather, especially for a long period of time. It happens most often in older adults and in people with ongoing health conditions.

• #11 Heat Stroke: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/166320-overview

  Heat illness may be viewed as a continuum of illnesses relating to the body’s inability to cope with heat. It includes minor illnesses, such as heat edema, heat rash (ie, prickly heat), heat cramps, heat tetany, as well as heat syncope and heat exhaustion. Heat stroke is the most severe heat-related illness and is defined as a body temperature higher than 40C (104F) associated with neurologic dysfunction. […] Heat stroke is defined as hyperthermia exceeding 40C (104F) associated with an altered sensorium. […] Despite wide variations in ambient temperatures, humans and other mammals can maintain a constant body temperature by balancing heat gain with heat loss. When heat gain overwhelms the body’s mechanisms of heat loss, the body temperature rises, potentially leading to heat stroke. Excessive heat denatures proteins, destabilizes phospholipids and lipoproteins, and liquefies membrane lipids, leading to cardiovascular collapse, multiorgan failure, and, ultimately, death.

• #12

  https://www.nursingcenter.com/journalarticle?Article_ID=593951&Journal_ID=230572&Issue_ID=593907

  Exposure to excessive heat may cause illness, as heat directly induces tissue injury, the severity of which is dependent upon the critical thermal maximum (ie, the level and duration of core heating). […] The critical thermal maximum in humans is a body temperature of 41.6[degrees]C to 42[degrees]C for between 45 minutes and 8 hours. […] The pathophysiologic sequence of events in HS is similar to that found in severe sepsis.

• #13 Heat stroke in children – UpToDate

  https://www.uptodate.com/contents/heat-stroke-in-children

  As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation to allow for reduction of body heat. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. Above 42°C (108°F), oxidative phosphorylation becomes uncoupled and a variety of enzymes cease to function. […] These pathophysiologic changes result in a systemic inflammatory response that causes multiple organ dysfunction and injury. […] The critical thermal maximum (CTM) is defined as the degree of elevated body temperature and duration of heat exposure that can be tolerated before cell damage occurs. […] Physiologic heat stress causes cell injury through several proposed mechanisms: Production of acute-phase reactants (eg, cytokines) that initiate an inflammatory cascade; Direct injury to cells with denaturation of proteins; Direct injury to the vascular endothelium resulting in impaired microcirculation and disseminated intravascular coagulation; Intestinal ischemia and increased permeability followed by endotoxemia.

• #14 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.

• #15 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.

• #16 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.

• #17 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  The leaky gut hypothesis has been linked to EHS pathophysiology because of observations that in patients with extreme EHS, high levels of lipopolysaccharide (a cell wall component of Gram negative bacteria) are observed. […] Systemic inflammatory response syndrome is a dysregulated defence response of the body to a noxious stressor to localise and eliminate the source of the insult. […] EHS is accompanied by a strong inflammatory response that leads to systemic inflammatory response syndrome and multi-organ damage. […] Coagulation is the process of changing the physical state of the blood from liquid to semi-solid. […] Disseminated intravascular coagulation has been reported in patients with EHS. […] EHS pathophysiology is complex and involves an interaction of thermoregulatory and cardiovascular factors that lead to systemic inflammatory response syndrome.

• #18 Protective mechanism of Xuebijing injection against heat stroke in rats

  https://www.spandidos-publications.com/10.3892/etm.2014.1639

  Heat stroke (HS) is a type of nerve damage caused by thermoregulatory dysfunction and excessive accumulation of body heat due to high temperature. The clinical symptoms mainly include high fever, no sweat and central nervous system disorders (1,2). HS is the most severe form of heat stress, with extensive damage to the body, and may lead to functional and morphological changes of numerous organs and systems. Once HS occurs, the mortality rate is as high as 63%, unless timely and proper treatment is received (3). […] The pathophysiological process of HS is similar to that of severe sepsis. Cytokines may mediate the systemic inflammatory response, and play key roles in the process of HS (4). The uncontrolled systemic inflammatory response causes a cascade resulting in multiple organ dysfunction syndrome (MODS). Bouchama and Knochel (1) consider that the characteristic pathological and clinical manifestations of HS are the interaction results of complex physiological and biochemical mechanisms prior to body collapse, including thermoregulatory imbalance, enlargement of the acute-phase response and the expression of heat shock protein (HSP).

• #19 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment. As core temperature rises, the preoptic nucleus of the anterior hypothalamus stimulates efferent fibers of the autonomic nervous system to produce sweating and cutaneous vasodilation. […] Temperature elevation is accompanied by an increase in oxygen consumption and metabolic rate, resulting in hyperpnea and tachycardia. A cytokine-mediated systemic inflammatory response develops, and the production of heat-shock proteins is increased. Blood is shunted from the splanchnic circulation to the skin and muscles, resulting in gastrointestinal ischemia and increased permeability of the intestinal mucosa. Hepatocytes, vascular endothelium, and neural tissue are most sensitive to increased core temperatures, but all organs may ultimately be involved. In severe cases, patients develop multi-organ-system failure and disseminated intravascular coagulation (DIC). Above 42°C (108°F), oxidative phosphorylation becomes uncoupled, and a variety of enzymes cease to function.

• #20 Heat stroke – Wikipedia

  https://en.wikipedia.org/wiki/Heat_stroke

  Growing evidence also suggests the existence of a second pathway underlying heat stroke that involves heat and exercise-driven endotoxemia. Although its exact mechanism is not yet fully understood, this model theorizes that extreme exercise and heat disrupt the intestinal barrier by making it more permeable and allowing lipopolysaccharides (LPS) from gram-negative bacteria within the gut to move into the circulatory system. High blood LPS levels can then trigger a systemic inflammatory response and eventually lead to sepsis and related consequences like blood coagulation, multi-organ failure, necrosis, and central nervous system dysfunction.

• #21 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  A person’s ability to thermoregulate is closely linked to the ability of the cardiovascular system to cope with central and peripheral blood flow demands to support metabolic and thermoregulatory requirements. […] Effective thermoregulatory pathways must be active to provide means for heat loss to prevent EHS during severe or prolonged physical activity. […] A thermoregulatory failure underlying EHS would signify a suppressed ability to dissipate heat coupled with high rates of heat storage, which would result in a marked elevation in core temperature. […] Increased intestinal permeability, also known as the leaky gut hypothesis, suggests that bacteria and toxins leak from the gut lumen, where they are normally contained via tight junctions, through the intestinal wall into the portal and general circulation.

• #22 Heat kills in 3 main ways. Know the signs to protect yourself : Shots – Health News : NPR

  https://www.npr.org/sections/health-shots/2023/07/23/1189506023/heres-what-happens-to-the-body-in-extreme-temperatures-and-how-heat-becomes-dead

  Of all extreme weather conditions, heat is the most deadly. It kills more people in the U.S. in an average year than hurricanes, tornadoes and floods combined. The human body has a built-in cooling mechanism sweat. But that system can only do so much, especially in soaring temperatures with high humidity. […] When your body is exposed to heat, it will try to cool itself down by redirecting more blood to the skin, says Ollie Jay, a professor of heat and health at the University of Sydney, where he directs the Heat and Health Research Incubator. But that means less blood and less oxygen are going to your gut. If these conditions go on long enough, your gut can become more permeable. […] „So, nasty things like endotoxins that usually reside and stay inside the gut start leaking out of the gut, entering the circulation. And that sets off a cascade of effects that ultimately result in death,” Jay says.

• #23 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  The leaky gut hypothesis has been linked to EHS pathophysiology because of observations that in patients with extreme EHS, high levels of lipopolysaccharide (a cell wall component of Gram negative bacteria) are observed. […] Systemic inflammatory response syndrome is a dysregulated defence response of the body to a noxious stressor to localise and eliminate the source of the insult. […] EHS is accompanied by a strong inflammatory response that leads to systemic inflammatory response syndrome and multi-organ damage. […] Coagulation is the process of changing the physical state of the blood from liquid to semi-solid. […] Disseminated intravascular coagulation has been reported in patients with EHS. […] EHS pathophysiology is complex and involves an interaction of thermoregulatory and cardiovascular factors that lead to systemic inflammatory response syndrome.

• #24 Heatstroke-Induced Inflammatory Response and Therapeutic Biomarkers

  https://www.mdpi.com/2227-9059/13/2/261

  Notably, an increased circulatory concentration of cytokines including IL-1α, IL-1β, soluble IL-6 receptor (sIL-6R), IL-6, IL-8, IL-10, IL-12, IFN-γ, tumor necrosis factor (TNF-α), and sTNFR has been reported during the heatstroke and becomes normal shortly after cooling. […] Overall, SIRS with other associated immune modulation during heatstroke causes DIC, leading to multiple organ failure, and even death. […] Additionally, the gut–brain barrier becomes permeable during heatstroke, allowing the migration of bacterial endotoxins and lipopolysaccharides to the circulatory system and ultimately to the brain, which causes neuroinflammation. […] In conclusion, endotoxemia and enhanced LPS levels are suggested to be involved in the induction of inflammatory response during heatstroke. […] Overall, the function of cytokines in SIRS, DIC, and the role of gut–brain axis dysbiosis in heatstroke need to be further explored.

• #25 Heatstroke-Induced Inflammatory Response and Therapeutic Biomarkers

  https://www.mdpi.com/2227-9059/13/2/261

  Notably, an increased circulatory concentration of cytokines including IL-1α, IL-1β, soluble IL-6 receptor (sIL-6R), IL-6, IL-8, IL-10, IL-12, IFN-γ, tumor necrosis factor (TNF-α), and sTNFR has been reported during the heatstroke and becomes normal shortly after cooling. […] Overall, SIRS with other associated immune modulation during heatstroke causes DIC, leading to multiple organ failure, and even death. […] Additionally, the gut–brain barrier becomes permeable during heatstroke, allowing the migration of bacterial endotoxins and lipopolysaccharides to the circulatory system and ultimately to the brain, which causes neuroinflammation. […] In conclusion, endotoxemia and enhanced LPS levels are suggested to be involved in the induction of inflammatory response during heatstroke. […] Overall, the function of cytokines in SIRS, DIC, and the role of gut–brain axis dysbiosis in heatstroke need to be further explored.

• #26 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w

  Cytokines are considered to be key mediators of SIRS in HS-induced systemic MODS and are closely related to the severity and outcome of HS. […] As one of the most ubiquitous, abundant, and evolutionarily conserved transcription and growth factors in eukaryotes, high mobility group box 1 (HMGB1) occupies an important position in the diagnosis and treatment of HS. […] The most common pathological change of HS-induced liver injury is the massive degeneration of hepatocytes including abnormal cell death, while pyroptosis exerts an important role in abnormal cell death in HS-induced liver injury. […] Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury.

• #27 Protective mechanism of Xuebijing injection against heat stroke in rats

  https://www.spandidos-publications.com/10.3892/etm.2014.1639

  The results of the present study show that under a high temperature environment, rats present with tissue ischemia and damage (increases in the levels of Cr, BUN, AST, ALT and ALP), organ dysfunction (changes in the MAP and HR), hypercoagulable state or disseminated intravascular coagulation (DIC) (increases in the levels of APTT, PT, FDP and D-D) and an excessively activated systemic inflammatory response (increases in the levels of IL-1, IL-6 and TNF-). However, pretreatment with XBJ prior to the beginning of heat stress significantly inhibited the HS-induced systemic inflammatory response, tissue ischemia and damage, and organ dysfunction, thus extending the survival time of the rats. […] IL-1, IL-6 and TNF- play crucial roles in the occurrence and development of HS (2). IL-1 is an endogenous pyrogen, which induces the inflammatory reaction in the acute period, with antitumor effects similar to those of tumor necrosis factors (14,15). It has been identified that the morbidity and mortality of HS are closely associated with endotoxemia and the release of IL-1 (16).

• #28 Heatstroke-Induced Inflammatory Response and Therapeutic Biomarkers

  https://www.mdpi.com/2227-9059/13/2/261

  This response is regulated by the heat-shock protein family and ultimately results in altered levels of pro-inflammatory and anti-inflammatory cytokines in plasma and tissues. […] In the case of long-term hyperthermia, this inflammatory response becomes uncontrolled and results in acute physiological conditions such as hypoxia, circulatory failure, and higher metabolic demands along with direct heat-associated cytotoxicity. […] The heatstroke-associated inflammatory response is equivalent to the systemic inflammatory response syndrome (SIRS). […] Interestingly, SIRS is regulated by circulating messenger RNAs that stimulate the release of cytokines and high-mobility group box 1 protein (HMGB1), which in turn causes the overactivation of leukocytes (monocytes, and macrophages) and endothelial cells.

• #29 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w

  Cytokines are considered to be key mediators of SIRS in HS-induced systemic MODS and are closely related to the severity and outcome of HS. […] As one of the most ubiquitous, abundant, and evolutionarily conserved transcription and growth factors in eukaryotes, high mobility group box 1 (HMGB1) occupies an important position in the diagnosis and treatment of HS. […] The most common pathological change of HS-induced liver injury is the massive degeneration of hepatocytes including abnormal cell death, while pyroptosis exerts an important role in abnormal cell death in HS-induced liver injury. […] Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury.

• #30 Heat stroke pathophysiology – wikidoc

  https://www.wikidoc.org/index.php/Heat_stroke_pathophysiology

  Heat-shock proteins are secreted in response to heat to protect cells from injury. Heat-shock proteins bind to proteins and act as chaperons to prevent them from denaturation. […] Severe heat stroke causes vascular congestion and/or hemorrhage, thrombi, increased inflammatory cells, and disruption of architecture in many internal organs including: liver, jejunum, spleen, lungs, and kidneys.

• #31 Heat Stroke: Practice Essentials, Pathophysiology, Etiology

  https://emedicine.medscape.com/article/166320-overview

  On a cellular level, heat directly influences the body by interfering with cellular processes along with denaturing proteins and cellular membranes. In turn, an array of inflammatory cytokines, interleukins and heat shock proteins (HSPs) are produced. In particular, HSP-70 allows the cell to endure the stress of its environment. Intense heat stress that is uncompensated leads to apoptosis and cell death. […] On a microvascular level, heat stroke resembles sepsis and involves inflammation, translocation of lipopolysaccharides from the gut, and activates the coagulation cascade. Certain preexisting factors, such as age, genetic makeup, and the nonacclimatized individual, may allow progression from heat stress to heat stroke, systemic inflammatory response syndrome (SIRS), multiorgan dysfunction syndrome (MODS), and ultimately death. Progression to heat stroke may occur through thermoregulatory failure, an amplified acute-phase response, and alterations in the expression of HSPs.

• #32

  https://www.nursingcenter.com/journalarticle?Article_ID=593951&Journal_ID=230572&Issue_ID=593907

  Heat stroke (HS) is a serious and potentially life-threatening condition defined as a core body temperature 40.6[degrees]C. […] Current understanding of HS indicates that it is due to thermoregulatory failure in addition to an exaggerated acute-phase response and altered genetic expression of heat-shock proteins. […] The progression from heat stress to HS is due to a combination of events including: thermoregulatory failure, an exaggerated acute-phase response to heat, and alteration in the production of heat-shock proteins. […] The acute-phase response to heat involves endothelial cells, leukocyte response, and epithelial cells. […] The third event in the progression of heat stress to HS involves the production of heat-shock proteins. […] When the synthesis of heat-shock proteins is blocked or altered, as in a genetic polymorphism, at the gene transcription level or by antibodies, the cells are rendered extremely sensitive to heat stress.

• #33 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  Subsequent inadequate water repletion may lead to substantial electrolyte abnormalities. Primarily, normonatremia or hypernatremia dehydration follows. If severe enough, it may lead to hemorrhage, brain edema, and permanent brain damage. Rarely, hyponatremia occurs following overcompensation with hypotonic fluid repletion, as seen in marathon runners and other exertional heat stroke populations. […] Hyperkalemia has been associated with heat stroke, which occurs when potassium is released from muscle breakdown or acidosis, causing a shift of potassium from cells to plasma. Potassium is a potent vasodilator in skeletal and cardiac muscle, and severe reductions in this electrolyte lead to cardiovascular instability and reduced muscle blood flow that predisposes to rhabdomyolysis. […] There is also a range of coagulopathies associated with heat stroke, from simple activation of the coagulation cascade and fibrinolysis to fatal hemorrhage or disseminated intravascular coagulation. Endothelial damage from heat is thought to cause downstream effects that result in platelet aggregation and microvascular thrombosis predisposing to consumptive coagulation, which paradoxically causes bleeding when platelets get used quicker than the body’s ability to produce them.

• #34 Heat stroke | Journal of Intensive Care | Full Text

  https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-018-0298-4

  Heat stroke is a life-threatening injury requiring neurocritical care; however, heat stroke has not been completely examined due to several possible reasons, such as no universally accepted definition or classification, and the occurrence of heat wave victims every few years. […] Heat stroke is a condition of multiple organ failure caused by hot environment. […] Hyperthermia due to passive heat exposure facilitates the leakage of endotoxin from the intestinal mucosa to the systemic circulation as well as the movement of interleukin (IL)-1 or IL-6 proteins from the muscles to the systemic circulation. […] The inflammatory and coagulation responses to heat stroke, together with direct cytotoxic effects of heat, injure the vascular endothelium, causing microthromboses. […] Heat stroke also suppresses platelet release from bone marrow due to megakaryocyte susceptibility to high temperature exposures. […] Heat stroke-induced coagulation activation and fibrin formation clinically manifest DIC.

• #35

  https://www.vin.com/apputil/content/defaultadv1.aspx?pId=22915&catId=124655&id=8896657&ind=419&objTypeID=17

  Heatstroke is caused by the inability to dissipate accumulated heat. In dogs it is characterized by core temperatures above 105.8F (41C) with CNS dysfunction. It results from exposure to a hot and humid environment or from strenuous physical exercise. Activation of inflammatory and haemostatic pathways initiates a systemic inflammatory response syndrome (SIRS) which often progresses to multi-organ dysfunction syndrome (MODS). Serious complications of heatstroke include rhabdomyolysis, acute kidney injury (AKI), acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). […] High body temperatures initiate a myriad of inflammatory, coagulation, and tissue damage processes, varying in severity and progression between dogs. Thermal endothelial cell injury leads to diffuse vascular damage and initiation of coagulation and subsequent microvascular thrombosis. In addition, multiorgan cellular necrosis further stimulates the coagulation system and results in DIC, an important factor in the morbidity and mortality of heatstroke patients. The injured endothelium releases thromboplastin and factor XII, which activates coagulation and the complement cascade, inducing SIRS and widespread DIC.

• #36 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  Subsequent inadequate water repletion may lead to substantial electrolyte abnormalities. Primarily, normonatremia or hypernatremia dehydration follows. If severe enough, it may lead to hemorrhage, brain edema, and permanent brain damage. Rarely, hyponatremia occurs following overcompensation with hypotonic fluid repletion, as seen in marathon runners and other exertional heat stroke populations. […] Hyperkalemia has been associated with heat stroke, which occurs when potassium is released from muscle breakdown or acidosis, causing a shift of potassium from cells to plasma. Potassium is a potent vasodilator in skeletal and cardiac muscle, and severe reductions in this electrolyte lead to cardiovascular instability and reduced muscle blood flow that predisposes to rhabdomyolysis. […] There is also a range of coagulopathies associated with heat stroke, from simple activation of the coagulation cascade and fibrinolysis to fatal hemorrhage or disseminated intravascular coagulation. Endothelial damage from heat is thought to cause downstream effects that result in platelet aggregation and microvascular thrombosis predisposing to consumptive coagulation, which paradoxically causes bleeding when platelets get used quicker than the body’s ability to produce them.

• #37 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  Subsequent inadequate water repletion may lead to substantial electrolyte abnormalities. Primarily, normonatremia or hypernatremia dehydration follows. If severe enough, it may lead to hemorrhage, brain edema, and permanent brain damage. Rarely, hyponatremia occurs following overcompensation with hypotonic fluid repletion, as seen in marathon runners and other exertional heat stroke populations. […] Hyperkalemia has been associated with heat stroke, which occurs when potassium is released from muscle breakdown or acidosis, causing a shift of potassium from cells to plasma. Potassium is a potent vasodilator in skeletal and cardiac muscle, and severe reductions in this electrolyte lead to cardiovascular instability and reduced muscle blood flow that predisposes to rhabdomyolysis. […] There is also a range of coagulopathies associated with heat stroke, from simple activation of the coagulation cascade and fibrinolysis to fatal hemorrhage or disseminated intravascular coagulation. Endothelial damage from heat is thought to cause downstream effects that result in platelet aggregation and microvascular thrombosis predisposing to consumptive coagulation, which paradoxically causes bleeding when platelets get used quicker than the body’s ability to produce them.

• #38 Canine Heat Stroke| Iowa Veterinary Specialties

  https://www.iowaveterinaryspecialties.com/student-scholars/canine-heat-stroke-literature-review

  Heat stroke results from failure of thermoregulation followed by an exaggerated acute phase response, alteration of heat shock proteins, and complications with the cardiovascular system. This leads to the production of reactive oxygen species, increased vascular and intestinal permeability, resulting in direct cellular injury and enzyme destruction. […] An overheated body will also attempt to cool itself by increasing cardiac output. The baroreceptor response first mediates peripheral vasodilation. This is an attempt by the body to dissipate heat via radiation where heat is passively transferred away from an overheated animal. […] Hyperthermia can lead to all the components of Virchows triad which includes vascular endothelial injury, venous stasis, and a hypercoagulable state. Widespread endothelial damage exposes subendothelial collagen and tissue factor which systemically activates platelets.

• #39 Canine Heat Stroke| Iowa Veterinary Specialties

  https://www.iowaveterinaryspecialties.com/student-scholars/canine-heat-stroke-literature-review

  Heat stroke results from failure of thermoregulation followed by an exaggerated acute phase response, alteration of heat shock proteins, and complications with the cardiovascular system. This leads to the production of reactive oxygen species, increased vascular and intestinal permeability, resulting in direct cellular injury and enzyme destruction. […] An overheated body will also attempt to cool itself by increasing cardiac output. The baroreceptor response first mediates peripheral vasodilation. This is an attempt by the body to dissipate heat via radiation where heat is passively transferred away from an overheated animal. […] Hyperthermia can lead to all the components of Virchows triad which includes vascular endothelial injury, venous stasis, and a hypercoagulable state. Widespread endothelial damage exposes subendothelial collagen and tissue factor which systemically activates platelets.

• #40 Heat stroke | Journal of Intensive Care | Full Text

  https://jintensivecare.biomedcentral.com/articles/10.1186/s40560-018-0298-4

  Heat stroke is a life-threatening injury requiring neurocritical care; however, heat stroke has not been completely examined due to several possible reasons, such as no universally accepted definition or classification, and the occurrence of heat wave victims every few years. […] Heat stroke is a condition of multiple organ failure caused by hot environment. […] Hyperthermia due to passive heat exposure facilitates the leakage of endotoxin from the intestinal mucosa to the systemic circulation as well as the movement of interleukin (IL)-1 or IL-6 proteins from the muscles to the systemic circulation. […] The inflammatory and coagulation responses to heat stroke, together with direct cytotoxic effects of heat, injure the vascular endothelium, causing microthromboses. […] Heat stroke also suppresses platelet release from bone marrow due to megakaryocyte susceptibility to high temperature exposures. […] Heat stroke-induced coagulation activation and fibrin formation clinically manifest DIC.

• #41 Protective mechanism of Xuebijing injection against heat stroke in rats

  https://www.spandidos-publications.com/10.3892/etm.2014.1639

  The results of the present study show that under a high temperature environment, rats present with tissue ischemia and damage (increases in the levels of Cr, BUN, AST, ALT and ALP), organ dysfunction (changes in the MAP and HR), hypercoagulable state or disseminated intravascular coagulation (DIC) (increases in the levels of APTT, PT, FDP and D-D) and an excessively activated systemic inflammatory response (increases in the levels of IL-1, IL-6 and TNF-). However, pretreatment with XBJ prior to the beginning of heat stress significantly inhibited the HS-induced systemic inflammatory response, tissue ischemia and damage, and organ dysfunction, thus extending the survival time of the rats. […] IL-1, IL-6 and TNF- play crucial roles in the occurrence and development of HS (2). IL-1 is an endogenous pyrogen, which induces the inflammatory reaction in the acute period, with antitumor effects similar to those of tumor necrosis factors (14,15). It has been identified that the morbidity and mortality of HS are closely associated with endotoxemia and the release of IL-1 (16).

• #42 Outcomes of Patients with Heatstroke and Heat Exhaustion | OAEM

  https://www.dovepress.com/a-systematic-review-on-outcomes-of-patients-with-heatstroke-and-heat-e-peer-reviewed-fulltext-article-OAEM

  Heatstroke (HS) is a severe form of heat-related illness (HRI) associated with high morbidity and mortality, representing a condition that includes long-term multiorgan dysfunction and susceptibility to further heat illness. […] A hallmark symptom of heat stroke is CNS dysfunction (a hallmark sign of HS) which manifests as mental status changes, including agitation, delirium, epilepsy, or coma at the time of the collapse. […] Severe heat stroke tends to be complicated by rhabdomyolysis, especially in patients with exertional heat stroke. Rhabdomyolysis may lead to systemic effects, including the local occurrence of compartment syndrome, hyperkalemic cardiac arrest, and/or lethal disseminated intravascular coagulopathy. […] Untreated heat stroke might exacerbate psychosis, lactic acidosis, consumptive coagulopathy, hematuria, pulmonary edema, renal failure, and other metabolic abnormalities.

• #43 Heat stroke | MedLink Neurology

  https://www.medlink.com/articles/heat-stroke

  Several cytokines are produced in response to acute heat stress. These mediate an inflammatory response with fever, leukocytosis, muscle catabolism, and stimulation of the hypothalamic-pituitary-adrenal axis. […] Long-term consequences of heat stroke are due to a systemic inflammatory response syndrome that may lead to multi-organ dysfunction and death. […] The central nervous system is particularly vulnerable to heat stroke. […] Heat stroke is associated with cerebral ischemia as well as increased levels of interleukin-1beta, dopamine, and glutamate in the brain. […] The cause of death in heat stroke is probably not CNS damage but systemic hemodynamic deterioration.

• #44 Heat stroke with neurological involvement | Neurology perspectives

  https://www.elsevier.es/en-revista-neurology-perspectives-17-avance-resumen-heat-stroke-with-neurological-involvement-S266704962200059X

  Heat stroke is a medical emergency characterised by a systemic inflammatory response secondary to an increase in body temperature above 40C, with severe multiple organ involvement, including the central nervous system (CNS), which is particularly vulnerable to hyperthermia. Heat stroke may be fatal or cause irreversible lesions. Though infrequent, its incidence is expected to increase due to the increasing frequency of heat waves. […] The pathophysiological mechanism of CNS damage and the related imaging findings is not well established, but is believed to be multifactorial, involving lesions secondary to direct thermal injury, as in the case of destruction of cerebellar Purkinje cells, as well as alterations in brain perfusion, with vasodilation, potentially leading to brain oedema, and subsequent vasoconstriction secondary to hypovolaemia, causing ischaemic damage and microvascular alterations similar to those occurring in disseminated intravascular coagulation, in association with brain haemorrhages.

• #45 Heat stroke with neurological involvement | Neurology perspectives

  https://www.elsevier.es/en-revista-neurology-perspectives-17-avance-resumen-heat-stroke-with-neurological-involvement-S266704962200059X

  Heat stroke is a medical emergency characterised by a systemic inflammatory response secondary to an increase in body temperature above 40C, with severe multiple organ involvement, including the central nervous system (CNS), which is particularly vulnerable to hyperthermia. Heat stroke may be fatal or cause irreversible lesions. Though infrequent, its incidence is expected to increase due to the increasing frequency of heat waves. […] The pathophysiological mechanism of CNS damage and the related imaging findings is not well established, but is believed to be multifactorial, involving lesions secondary to direct thermal injury, as in the case of destruction of cerebellar Purkinje cells, as well as alterations in brain perfusion, with vasodilation, potentially leading to brain oedema, and subsequent vasoconstriction secondary to hypovolaemia, causing ischaemic damage and microvascular alterations similar to those occurring in disseminated intravascular coagulation, in association with brain haemorrhages.

• #46 Heat stroke with neurological involvement | Neurology perspectives

  https://www.elsevier.es/en-revista-neurology-perspectives-17-avance-resumen-heat-stroke-with-neurological-involvement-S266704962200059X

  These findings are compatible with ischaemic and haemorrhagic processes in the context of heat stroke. […] Heat stroke has also been reported to cause cerebral venous thrombosis. […] The largest series of patients undergoing MRI studies was published by Shimada et al. in 2019, with a review of 22 previously published cases plus 2 new cases. The authors classified MRI findings as infarction-like lesions or posterior reversible encephalopathy syndrome-like lesions, due to the pathophysiological similarities and associated vascular regulation alterations; 4 patients presented both types of MRI lesions. […] The initial CT scan of patients with heat stroke usually detects no abnormalities, or only indirect signs of brain oedema; however, CT is performed in the majority of cases to rule out potentially treatable lesions. Patients with persistent neurological symptoms may be assessed with MRI, with T2-weighted or FLAIR sequences to evaluate ischaemic or haemorrhagic small-vessel lesions and DWI and ADC sequences to detect cytotoxic oedema, which is linked to irreversible neuronal damage. Contrast-enhanced sequences reveal blood-brain barrier disruption secondary to vascular and/or inflammatory processes.

• #47 Heat Stroke and the SLPs Role – Carolina Speech Pathology

  https://carolinafees.com/heat-stroke-and-the-slps-role/

  Heat stroke is the most serious heat-related disorder. Heat stroke occurs when the body is unable to control its own temperature. As body temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. […] Heat stroke can cause permanent disability and even death if not treated immediately. […] This is due to the possibility of neurological complications following heat stroke, typically manifested as cerebellar ataxia, cognitive impairment, dysphagia, and aphasia. […] Although complete neurological recovery does occur in some survivors of heat stroke, deficits may persist in 20% of cases since the cerebellum is the most susceptible to thermal damage. […] Clinical features are usually bilateral, and recovery may be minimal or absent. […] Cerebellar atrophy was also reported 10 weeks following heat stroke events, with progressive atrophy noted during a 1 year follow up. […] Speech language pathologists should be consulted to address persistent neurological deficits following heat stroke and can expect to encounter issues similar to cerebral vascular accidents: dysarthria, aphasia, cognitive deficits, and dysphagia.

• #48 Canine Heat Stroke| Iowa Veterinary Specialties

  https://www.iowaveterinaryspecialties.com/student-scholars/canine-heat-stroke-literature-review

  The hallmark sign of heat stress is severe central nervous system disturbance and it is often associated with multiple organ dysfunction. The combination of poor perfusion, direct thermal damage, cerebral edema, and hemorrhage all contribute to the central nervous system symptoms. […] Acute renal failure and hepatic failure is a result of direct thermal injury, hypoxia, and microthrombi from DIC. Rhabdomyolysis occurs as a direct result of high temperature and may be increased in patients experiencing an exertional heat stroke. […] Many of the heatstroke sequelae are mediated by an out of control acute phase inflammatory response.

• #49 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w

  Cytokines are considered to be key mediators of SIRS in HS-induced systemic MODS and are closely related to the severity and outcome of HS. […] As one of the most ubiquitous, abundant, and evolutionarily conserved transcription and growth factors in eukaryotes, high mobility group box 1 (HMGB1) occupies an important position in the diagnosis and treatment of HS. […] The most common pathological change of HS-induced liver injury is the massive degeneration of hepatocytes including abnormal cell death, while pyroptosis exerts an important role in abnormal cell death in HS-induced liver injury. […] Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury.

• #50 The pathogenesis and therapeutic strategies of heat stroke-induced liver injury | Critical Care | Full Text

  https://ccforum.biomedcentral.com/articles/10.1186/s13054-022-04273-w

  Cytokines are considered to be key mediators of SIRS in HS-induced systemic MODS and are closely related to the severity and outcome of HS. […] As one of the most ubiquitous, abundant, and evolutionarily conserved transcription and growth factors in eukaryotes, high mobility group box 1 (HMGB1) occupies an important position in the diagnosis and treatment of HS. […] The most common pathological change of HS-induced liver injury is the massive degeneration of hepatocytes including abnormal cell death, while pyroptosis exerts an important role in abnormal cell death in HS-induced liver injury. […] Excessive ROS will be produced during heat stress, which has been proven to be a key stimulator of NLRP3 inflammasome and a potential target for negative regulation of cell pyroptosis. […] The previous studies have suggested that mitophagy is closely related to the occurrence and development of various liver diseases, including viral hepatitis, liver ischemia/reperfusion (I/R) injury, and drug-induced liver injury.

• #51 Management of exertional heat stroke: a practical update for primary care physicians | British Journal of General Practice

  https://bjgp.org/content/68/668/153

  Patients should ideally be admitted to hospital for further assessment once cooling has occurred, for monitoring of multi-organ dysfunction. Heat illness is associated with renal failure in 13% of patients, exacerbated by rhabdomyolysis and dehydration, and may require renal replacement therapy. […] Although much of the multi-organ dysfunction is likely to be due to thermal damage, it has been suggested that translocation of gastrointestinal compounds may generate sepsis or a pro-inflammatory state.

• #52 Heat kills in 3 main ways. Know the signs to protect yourself : Shots – Health News : NPR

  https://www.npr.org/sections/health-shots/2023/07/23/1189506023/heres-what-happens-to-the-body-in-extreme-temperatures-and-how-heat-becomes-dead

  Mora notes another danger to the kidneys that people who work physically demanding jobs in high heat outdoors face. Rhabdomyolysis causes muscle tissue to break down, releasing proteins into the blood that can clog kidneys. This usually occurs in the acute phase of heatstroke. […] Jay says there’s also some evidence that habitually working outdoors in high heat without proper hydration can increase the risk of chronic kidney disease. […] If your core body temperature rises to about 104 degrees Fahrenheit, Jay says, that’s where you risk heatstroke. […] „The military has done a lot of research into heat exposure and they find the first symptoms of heat exhaustion, heatstroke after only a few hours, even among the healthiest of people,” Mora says.

• #53 The pathogenesis and management of heatstroke and heatstroke-induced lung injury

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11729746/

  The lung often acts as a vulnerable, affected, and injured organ in heatstroke due to its unique structure, and impaired lung function further promotes anoxic damage to other vital tissues and organs. […] Heat stress usually induces lung injury through direct thermal cytotoxic effects and secondary uncontrolled systemic inflammation. […] With the progress of research on heatstroke, secondary uncontrolled systemic inflammation is considered the main cause of lung injury in heatstroke patients. […] The above studies demonstrated that PMVEC damage caused by the local inflammatory response and oxidative stress is one of the key causes of heatstroke-induced lung injury. […] Heatstroke-induced lung injury involves ferroptosis in alveolar epithelial cells. […] Lung injury caused by heatstroke, heat damage to cells, and the excessive release of endotoxin and cytokines (TNF-, INF-, and IL-1) cause PMVEC damage, activate the coagulation system, induce the release of inflammatory factors, and activate tissue factor and the exogenous coagulation system.

• #54 The pathogenesis and management of heatstroke and heatstroke-induced lung injury

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11729746/

  The lung often acts as a vulnerable, affected, and injured organ in heatstroke due to its unique structure, and impaired lung function further promotes anoxic damage to other vital tissues and organs. […] Heat stress usually induces lung injury through direct thermal cytotoxic effects and secondary uncontrolled systemic inflammation. […] With the progress of research on heatstroke, secondary uncontrolled systemic inflammation is considered the main cause of lung injury in heatstroke patients. […] The above studies demonstrated that PMVEC damage caused by the local inflammatory response and oxidative stress is one of the key causes of heatstroke-induced lung injury. […] Heatstroke-induced lung injury involves ferroptosis in alveolar epithelial cells. […] Lung injury caused by heatstroke, heat damage to cells, and the excessive release of endotoxin and cytokines (TNF-, INF-, and IL-1) cause PMVEC damage, activate the coagulation system, induce the release of inflammatory factors, and activate tissue factor and the exogenous coagulation system.

• #55 The pathogenesis and management of heatstroke and heatstroke-induced lung injury

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11729746/

  The lung often acts as a vulnerable, affected, and injured organ in heatstroke due to its unique structure, and impaired lung function further promotes anoxic damage to other vital tissues and organs. […] Heat stress usually induces lung injury through direct thermal cytotoxic effects and secondary uncontrolled systemic inflammation. […] With the progress of research on heatstroke, secondary uncontrolled systemic inflammation is considered the main cause of lung injury in heatstroke patients. […] The above studies demonstrated that PMVEC damage caused by the local inflammatory response and oxidative stress is one of the key causes of heatstroke-induced lung injury. […] Heatstroke-induced lung injury involves ferroptosis in alveolar epithelial cells. […] Lung injury caused by heatstroke, heat damage to cells, and the excessive release of endotoxin and cytokines (TNF-, INF-, and IL-1) cause PMVEC damage, activate the coagulation system, induce the release of inflammatory factors, and activate tissue factor and the exogenous coagulation system.

• #56

  https://www.vin.com/apputil/content/defaultadv1.aspx?pId=22915&catId=124655&id=8896657&ind=419&objTypeID=17

  Heatstroke is caused by the inability to dissipate accumulated heat. In dogs it is characterized by core temperatures above 105.8F (41C) with CNS dysfunction. It results from exposure to a hot and humid environment or from strenuous physical exercise. Activation of inflammatory and haemostatic pathways initiates a systemic inflammatory response syndrome (SIRS) which often progresses to multi-organ dysfunction syndrome (MODS). Serious complications of heatstroke include rhabdomyolysis, acute kidney injury (AKI), acute respiratory distress syndrome (ARDS), and disseminated intravascular coagulation (DIC). […] High body temperatures initiate a myriad of inflammatory, coagulation, and tissue damage processes, varying in severity and progression between dogs. Thermal endothelial cell injury leads to diffuse vascular damage and initiation of coagulation and subsequent microvascular thrombosis. In addition, multiorgan cellular necrosis further stimulates the coagulation system and results in DIC, an important factor in the morbidity and mortality of heatstroke patients. The injured endothelium releases thromboplastin and factor XII, which activates coagulation and the complement cascade, inducing SIRS and widespread DIC.

• #57 Canine Heat Stroke| Iowa Veterinary Specialties

  https://www.iowaveterinaryspecialties.com/student-scholars/canine-heat-stroke-literature-review

  Heat stroke results from failure of thermoregulation followed by an exaggerated acute phase response, alteration of heat shock proteins, and complications with the cardiovascular system. This leads to the production of reactive oxygen species, increased vascular and intestinal permeability, resulting in direct cellular injury and enzyme destruction. […] An overheated body will also attempt to cool itself by increasing cardiac output. The baroreceptor response first mediates peripheral vasodilation. This is an attempt by the body to dissipate heat via radiation where heat is passively transferred away from an overheated animal. […] Hyperthermia can lead to all the components of Virchows triad which includes vascular endothelial injury, venous stasis, and a hypercoagulable state. Widespread endothelial damage exposes subendothelial collagen and tissue factor which systemically activates platelets.

• #58

  https://link.springer.com/article/10.1007/BF02911618

  Heat stroke model was made under artificial hot environment in 26 mongrel dogs, and hemodynamic alterations and their mechanism were investigated. […] These findings suggested that the circulatory failure during heat stroke might be related to the increased -endorphin release from the anterior pituitary gland and the increase of serum potassium concentration.

• #59

  https://link.springer.com/article/10.1007/BF02911618

  Heat stroke model was made under artificial hot environment in 26 mongrel dogs, and hemodynamic alterations and their mechanism were investigated. […] These findings suggested that the circulatory failure during heat stroke might be related to the increased -endorphin release from the anterior pituitary gland and the increase of serum potassium concentration.

• #60 Heat-related illnesses – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/heat-related-illnesses/

  Heat exhaustion, a moderate heat-related illness, is characterized by dehydration, normal or slightly elevated body temperature (typically 40C), and normal mental status. Clinical features include symptoms of dehydration, nausea, headache, weakness, and ataxia. […] Heatstroke is a life-threatening heat-related illness characterized by severe hyperthermia (with a body temperature typically 40C) and severe CNS dysfunction. The cornerstone of treatment is aggressive active cooling to reduce core body temperature to less than 40C. […] In hyperthermia, the hypothalamic thermoregulatory response is inadequate to maintain a normal temperature. High body temperature protein denaturation, phospholipid and lipoprotein damage, and membrane lipid liquefaction cell damage and loss of function (including myocardiocytes and neurons) cardiovascular collapse multi-organ failure and possibly death.

• #61 Heat Stroke vs. Heat Exhaustion: Key Differences

  https://health.clevelandclinic.org/heat-exhaustion-vs-heat-stroke

  Heat stroke is the most severe form of heat illness, with primary symptoms that include confusion, altered mental status and a very high core body temperature above 104 degrees Fahrenheit (40 degrees Celsius). […] Heat exhaustion is less dangerous, but can present with muscle cramps, headaches, dizziness, weakness, fatigue, nausea and vomiting. […] Heat exhaustion and heat stroke are types of heat-related illnesses. […] People often talk about heat exhaustion and heat stroke as though they are separate things. But they exist on a spectrum from not-so-serious to a significant and life-threatening emergency. […] Heat exhaustion occurs when your body cant cool itself through sweating. Untreated, it can progress to heat stroke. […] During heat stroke, your body temperature climbs quickly to dangerous levels. Often, people with heat stroke stop sweating. The bodys mechanisms for dealing with heat are overwhelmed. Without treatment, can be deadly.

• #62 Heat exhaustion – Knowledge and References – Taylor & Francis

  https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Emergency_medicine/Heat_exhaustion/

  Heat exhaustion is a condition that occurs when the body’s cooling mechanism fails to maintain a normal core temperature, resulting in profuse perspiration, clammy skin, dizziness, nausea, and muscle cramps. This condition is caused by the loss of large amounts of fluid through sweating, often accompanied by excessive loss of salt. […] Heat exhaustion is caused by a failure of the body’s cooling mechanism to maintain a normal core temperature. Symptoms of heat exhaustion include weakness, nausea, cramps, anxiety, excess sweating, syncope (fainting), rapid breathing, and a fast, weak pulse. These result in extreme exhaustion and an inability to exert oneself further. Heat exhaustion also results in water depletion or salt depletion and can lead to heatstroke, which is more serious and can be life threatening.

• #63 Heat-related illnesses – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/heat-related-illnesses/

  Heat exhaustion is a heat-related illness characterized by all of the following: Decrease in blood volume and/or total body water caused by heat stress, Normal or slightly elevated core body temperature (typically defined as 40C), Normal mental status. […] In contrast with heatstroke, the homeostatic thermoregulatory system retains partial function, and heat continues to actively dissipate. […] Heatstroke is a life-threatening heat-related illness characterized by all of the following: Significantly elevated core body temperature; typically defined as 40C (104F), Severe CNS dysfunction, e.g., encephalopathy, seizures, coma, Recent intense physical exertion and/or exposure to extreme heat.

• #64 Heat-related illnesses – Knowledge @ AMBOSS

  https://www.amboss.com/us/knowledge/heat-related-illnesses/

  Heat exhaustion is a heat-related illness characterized by all of the following: Decrease in blood volume and/or total body water caused by heat stress, Normal or slightly elevated core body temperature (typically defined as 40C), Normal mental status. […] In contrast with heatstroke, the homeostatic thermoregulatory system retains partial function, and heat continues to actively dissipate. […] Heatstroke is a life-threatening heat-related illness characterized by all of the following: Significantly elevated core body temperature; typically defined as 40C (104F), Severe CNS dysfunction, e.g., encephalopathy, seizures, coma, Recent intense physical exertion and/or exposure to extreme heat.

• #65 Heat Exhaustion: Symptoms, Causes, and Treatment | Red Cross

  https://www.redcross.org/take-a-class/resources/learn-first-aid/heat-exhaustion?srsltid=AfmBOors4iB1sWwRDEzaMiDfFWH06b0nWJXq6Ut6rEdZPMUbiJ4ZVEtV

  Heat exhaustion occurs when fluids lost through sweating are not replaced. The bodys primary mechanism of cooling itself is through sweating. […] Heat exhaustion is often accompanied by dehydration, as the bodys excessive production of sweat in an attempt to cool itself depletes fluid levels in the body. […] Yes. The first is not getting enough fluids. Heat exhaustion occurs when fluids lost through sweating are not replaced. The bodys primary mechanism of cooling itself is through sweating. As sweat evaporates from the body, it takes body heat with it, cooling the body. If a person does not take in enough fluids, the body does not have what it needs to make adequate amounts of sweat. Heat exhaustion is often accompanied by dehydration. […] Also, humid environments and environments without good air circulation can make it difficult for the sweat to evaporate. Under these conditions, a person may develop heat exhaustion.

• #66 Heat exhaustion – Knowledge and References – Taylor & Francis

  https://taylorandfrancis.com/knowledge/Medicine_and_healthcare/Emergency_medicine/Heat_exhaustion/

  Heat exhaustion is a condition that occurs when the body’s cooling mechanism fails to maintain a normal core temperature, resulting in profuse perspiration, clammy skin, dizziness, nausea, and muscle cramps. This condition is caused by the loss of large amounts of fluid through sweating, often accompanied by excessive loss of salt. […] Heat exhaustion is caused by a failure of the body’s cooling mechanism to maintain a normal core temperature. Symptoms of heat exhaustion include weakness, nausea, cramps, anxiety, excess sweating, syncope (fainting), rapid breathing, and a fast, weak pulse. These result in extreme exhaustion and an inability to exert oneself further. Heat exhaustion also results in water depletion or salt depletion and can lead to heatstroke, which is more serious and can be life threatening.

• #67 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health

  https://msdh.ms.gov/page/43,3942,98,261.html

  Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.

• #68 Heat stroke in children – UpToDate

  https://www.uptodate.com/contents/heat-stroke-in-children

  The diagnostic criteria for patients with heat stroke are elevated core temperature (≥40 to 40.5°C [104 to 105°F]) and central nervous system (CNS) abnormalities following environmental heat exposure. […] While the distinction between heat exhaustion and heat stroke is sometimes unclear, children with elevated body temperature and CNS abnormalities should be treated as victims of heat stroke, given the significant morbidity and mortality associated with this condition.

• #69 Heat Stress, Heat Stroke & Hypothermia | Emergency Management & Business Continuity | Western Washington University

  https://embc.wwu.edu/heat-stress-heat-stroke-hypothermia

  Heat stress is the bodys response to an excessive loss of the water and salt contained in sweat. If heat stress is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body is unable to regulate its temperature. During heat stroke, the bodys temperature rises, the sweating mechanism fails, and the body is unable to cool down.

• #70 Heat Exhaustion and Heat Stroke – Mississippi State Department of Health

  https://msdh.ms.gov/page/43,3942,98,261.html

  Heat exhaustion is a milder form of heat-related illness that can develop after long exposure to high temperatures and inadequate water. Those most prone to heat exhaustion are elderly people, people with high blood pressure, and people working or exercising in a hot environment. […] If heat exhaustion is untreated, it may progress to heat stroke. […] Heat stroke occurs when the body’s temperature rises rapidly, the sweating mechanism fails, and the body is unable to cool down. Body temperature may rise to 106 degrees or higher within 10 to 15 minutes. Heat stroke can cause death or permanent disability if emergency treatment is not provided.

• #71 The Difference Between Dehydration, Heat Exhaustion and Heat Stroke

  https://www.emoryhealthcare.org/stories/wellness/the-difference-between-dehydration-heat-exhaustion-and-heat-stroke

  Heat exhaustion is a serious condition. Heat exhaustion happens when the body loses a great deal of water and salt (which is usually caused by profuse sweating). Cases of heat exhaustion are made much worse whenever there is a high level of humidity or physical activity involved. Notably, heat exhaustion can cause any pre-existing conditions to worsen or become more apparent. It is important to know the signs of heat exhaustion, as it could take place within a very short period of time. […] Heat exhaustion left untreated may result in heat stroke. This is a life-threatening condition that can result in damage to the brain or other important organs. In some cases, heat stroke may cause multiple organ systems to fail and can ultimately cause death. During heat stroke, the body’s core temperature rises above 106 F within a time frame of 10 to 15 minutes. This rapid increase in body heat coupled with a failing sweating mechanism leaves the body without the ability to cool itself.

• #72 Heat stroke in children – UpToDate

  https://www.uptodate.com/contents/heat-stroke-in-children

  Heat stroke occurs in patients with environmental heat exposure and is defined as a core body temperature ≥40 to 40.5°C (104 to 105°F) accompanied by central nervous system (CNS) dysfunction. […] This condition represents a failure of the body’s ability to maintain thermoregulatory homeostasis. Heat stroke is further classified as follows: Classic (nonexertional) heat stroke – Classic heat stroke arises from environmental exposure to heat and is more common in younger children who are unable to escape from hot environments and those with underlying chronic medical conditions that impair thermoregulation. […] Exertional heat stroke generally occurs in young, otherwise healthy individuals who engage in heavy exercise during periods of high ambient temperature and humidity. […] Body temperature is maintained within a narrow range by balancing heat load with heat dissipation. The body’s heat load results from both metabolic processes and absorption of heat from the environment.

• #73 Heatstroke – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/heat-stroke/symptoms-causes/syc-20353581

  Heatstroke is a condition caused by the body overheating. This usually happens because of exposure to high temperatures or physical activity in high temperatures for too long. There are a few stages of heat injury, and heatstroke is the most serious. It can happen if body temperature rises to 104 F (40 C) or higher. Heatstroke needs emergency care. If it’s not treated, heatstroke can quickly damage the brain, heart, kidneys and muscles. This damage gets worse the longer treatment is delayed, which increases the risk of serious complications or death. […] Heatstroke can happen as a result of: Being in a hot environment. In a type of heatstroke, called nonexertional (classic) heatstroke, being in a hot environment leads to a rise in core body temperature. This type of heatstroke typically happens after exposure to hot, humid weather, especially for a long period of time. It happens most often in older adults and in people with ongoing health conditions.

• #74 Heatstroke – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/heat-stroke/symptoms-causes/syc-20353581

  Doing strenuous activity. Exertional heatstroke is caused by an increase in core body temperature brought on by intense physical activity in hot weather. Anyone exercising or working in hot weather can get exertional heatstroke, but it’s most likely to happen if you’re not used to high temperatures. […] In either type of heatstroke, your condition can be brought on by: Wearing heavy clothing that prevents sweat from evaporating easily and cooling the body. Drinking alcohol, which can affect the body’s ability to regulate temperature. Becoming dehydrated by not drinking enough water to replenish fluids lost through sweating. […] Heatstroke can result in a number of complications, depending on how long the body temperature is high. Serious complications include: Vital organ damage. Without a quick response to lower the body temperature, heatstroke can cause the brain or other vital organs to swell, possibly resulting in permanent damage. Death. Without prompt and adequate treatment, heatstroke can be fatal.

• #75 Nonexertional (classic) heat stroke in adults – UpToDate

  https://www.uptodate.com/contents/severe-nonexertional-hyperthermia-classic-heat-stroke-in-adults

  Heat stroke is defined as an elevated core body temperature, usually in excess of 40.5°C (105°F), with associated central nervous system (CNS) dysfunction in the setting of a large environmental heat load that cannot be dissipated. It is a potentially fatal condition that requires rapid identification and treatment. […] Patients who present to the hospital with nonexertional (classic) heat stroke have high mortality, with rates ranging from 21 to 63 percent. Mortality correlates with the degree of temperature elevation, time to initiation of cooling measures, and the number of organ systems affected. […] The diagnosis of nonexertional (classic) heat stroke is made clinically based upon an elevated core body temperature (generally >40.5°C [105°F]), central nervous system (CNS) dysfunction (eg, altered mental status), and exposure to severe environmental heat.

• #76 Heatstroke – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/heat-stroke/symptoms-causes/syc-20353581

  Doing strenuous activity. Exertional heatstroke is caused by an increase in core body temperature brought on by intense physical activity in hot weather. Anyone exercising or working in hot weather can get exertional heatstroke, but it’s most likely to happen if you’re not used to high temperatures. […] In either type of heatstroke, your condition can be brought on by: Wearing heavy clothing that prevents sweat from evaporating easily and cooling the body. Drinking alcohol, which can affect the body’s ability to regulate temperature. Becoming dehydrated by not drinking enough water to replenish fluids lost through sweating. […] Heatstroke can result in a number of complications, depending on how long the body temperature is high. Serious complications include: Vital organ damage. Without a quick response to lower the body temperature, heatstroke can cause the brain or other vital organs to swell, possibly resulting in permanent damage. Death. Without prompt and adequate treatment, heatstroke can be fatal.

• #77 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  Exertional heat stroke is characterised by central nervous system dysfunction in people with hyperthermia during physical activity and can be influenced by environmental factors such as heatwaves, which extend the incidence of exertional heat stroke beyond athletics only. […] The pathophysiology of exertional heat stroke involves thermoregulatory and cardiovascular overload, resulting in severe hyperthermia and subsequent multiorgan injury due to a systemic inflammatory response syndrome and coagulopathy. […] Understanding the pathophysiology and the risk factors that lead to EHS is important for the correct diagnosis and the choice of mitigation strategies. […] In this article, we will discuss four aspects of EHS pathophysiology: thermoregulatory or cardiovascular limitations, the so-called leaky gut hypothesis and endotoxaemia, inflammation and systemic inflammatory response syndrome, and coagulopathy and disseminated intravascular coagulation.

• #78 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  Exertional heat stroke is characterised by central nervous system dysfunction in people with hyperthermia during physical activity and can be influenced by environmental factors such as heatwaves, which extend the incidence of exertional heat stroke beyond athletics only. […] The pathophysiology of exertional heat stroke involves thermoregulatory and cardiovascular overload, resulting in severe hyperthermia and subsequent multiorgan injury due to a systemic inflammatory response syndrome and coagulopathy. […] Understanding the pathophysiology and the risk factors that lead to EHS is important for the correct diagnosis and the choice of mitigation strategies. […] In this article, we will discuss four aspects of EHS pathophysiology: thermoregulatory or cardiovascular limitations, the so-called leaky gut hypothesis and endotoxaemia, inflammation and systemic inflammatory response syndrome, and coagulopathy and disseminated intravascular coagulation.

• #79 Exertional heat stroke: pathophysiology and risk factors | BMJ Medicine

  https://bmjmedicine.bmj.com/content/1/1/e000239

  Exertional heat stroke is characterised by central nervous system dysfunction in people with hyperthermia during physical activity and can be influenced by environmental factors such as heatwaves, which extend the incidence of exertional heat stroke beyond athletics only. […] The pathophysiology of exertional heat stroke involves thermoregulatory and cardiovascular overload, resulting in severe hyperthermia and subsequent multiorgan injury due to a systemic inflammatory response syndrome and coagulopathy. […] Understanding the pathophysiology and the risk factors that lead to EHS is important for the correct diagnosis and the choice of mitigation strategies. […] In this article, we will discuss four aspects of EHS pathophysiology: thermoregulatory or cardiovascular limitations, the so-called leaky gut hypothesis and endotoxaemia, inflammation and systemic inflammatory response syndrome, and coagulopathy and disseminated intravascular coagulation.

• #80 Acute Management of Heat Stroke: Facts and Figures | IntechOpen

  https://www.intechopen.com/chapters/88937

  Heat-related illnesses range from heat exhaustion to heat stroke. Heat stroke is a life-threatening medical emergency causing multiple organ dysfunction that if not treated, can be fatal. It is a severe heat illness with a body temperature of more than 400c and organ dysfunction. […] Pathophysiology is exposure to higher temperatures with impaired thermoregulation. Patients will present with high core body temperature; tachypnea, tachycardia, and hypotension may be present. The manifestations of organ dysfunction range from coagulopathy to altered levels of consciousness, and pulmonary edema. […] The heat stroke thus generates inflammatory and coagulopathy responses; the direct effect of heat also causes endothelial injury and generates microthromboses, leading to a disseminated intravascular coagulation (DIC) response. […] Heat stroke generates a systemic inflammatory and coagulopathy response in combination with heat injury causes organ dysfunctions. Diagnosed with raised body temperature with clinical manifestation and signs and symptoms of organ dysfunction or failure.

• #81 Acute Management of Heat Stroke: Facts and Figures | IntechOpen

  https://www.intechopen.com/chapters/88937

  Heat-related illnesses range from heat exhaustion to heat stroke. Heat stroke is a life-threatening medical emergency causing multiple organ dysfunction that if not treated, can be fatal. It is a severe heat illness with a body temperature of more than 400c and organ dysfunction. […] Pathophysiology is exposure to higher temperatures with impaired thermoregulation. Patients will present with high core body temperature; tachypnea, tachycardia, and hypotension may be present. The manifestations of organ dysfunction range from coagulopathy to altered levels of consciousness, and pulmonary edema. […] The heat stroke thus generates inflammatory and coagulopathy responses; the direct effect of heat also causes endothelial injury and generates microthromboses, leading to a disseminated intravascular coagulation (DIC) response. […] Heat stroke generates a systemic inflammatory and coagulopathy response in combination with heat injury causes organ dysfunctions. Diagnosed with raised body temperature with clinical manifestation and signs and symptoms of organ dysfunction or failure.

• #82 Heat Stroke – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK537135/

  Management of heat stroke includes ensuring adequate airway protection, breathing, and circulation. After ABCs, rapid cooling becomes the mainstay of treatment with ancillary management in response to other end-organ damage. […] The use of dantrolene has been shown in several small trials to be ineffective and is not recommended in treating heat stroke. The use of benzodiazepines in heat stroke may have merit for a patient who is agitated and shivering; however, empiric treatment is inadvisable until further studies are undertaken. […] Finally, expedited rapid cooling has been shown in several RCT both directly and indirectly to be the most effective treatment to limit mortality in heatstroke.

• #83 Management of exertional heat stroke: a practical update for primary care physicians | British Journal of General Practice

  https://bjgp.org/content/68/668/153

  Exertional heat stroke (EHS) is a risk to athletes, the military, and others undergoing strenuous exertion, especially in temperate climates. It is defined as a core temperature of 40C with neurological impairment. It is one of the three commonest causes of deaths in athletes, and, untreated, the mortality may be up to 80%. Even when treated, it is associated with significant short- and long-term morbidity. […] Hyperthermia with a core temperature 40C, with neurocognitive dysfunction, is diagnostic however, cutaneous vasoconstriction may mean that a peripheral temperature measurement is inaccurately low. A core temperature measurement (using a rectal thermometer) is required on any collapsed athlete. […] Immediate cooling is the priority, along with maintaining a patent airway and adequate ventilation and circulation. Reducing the core temperature to below 38.9C within 60 minutes is associated with an improved survival.

• #84 The pathogenesis and management of heatstroke and heatstroke-induced lung injury

  https://pmc.ncbi.nlm.nih.gov/articles/PMC11729746/

  Although heatstroke- and sepsis-induced lung injuries are similar, there are essential differences between the two conditions. […] Hence, further investigating and comprehensively studying the mechanisms associated with heatstroke and heatstroke-induced lung injury holds immense importance for safeguarding humans from heatwaves.

• #85 Outcomes of Patients with Heatstroke and Heat Exhaustion | OAEM

  https://www.dovepress.com/a-systematic-review-on-outcomes-of-patients-with-heatstroke-and-heat-e-peer-reviewed-fulltext-article-OAEM

  Heat stroke has an indication of multiple health hazards like renal and diabetic problems are all linked with the illness of heat stroke. […] The phenomena have proved that heat stroke contributes to physiological and morphological complications. […] The researchers define HS based on pathophysiology which stated it as a form of hyperthermia accompanied by a systemic inflammatory response (SIR) resulting in multiorgan failure including rhabdomyolysis, renal failure, hepatitis, or coagulation disorder, particularly encephalopathy. […] In heat stroke, there is further impairment of thermoregulation due to a reduction in cutaneous vasodilation as a result of shunting of the blood from the central circulation to the muscles and skin, leading to MOF. […] This study concludes that HS is a life-threatening condition marked by neurological disorders, damage in the hepatic system, renal system, coagulation failure, muscular-skeletal system, and cardiovascular system. […] This review elucidated that core body temperature and white blood cell count are pivotal determinants influencing the outcomes of heat stroke. […] It is crucial to recognize the significance of novel biotechnologies in advancing our understanding of the pathophysiology of heat stroke.

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