Classification of Heatstroke
Pathogenesis
The hypothalamic thermoregulatory center controls heat production and dissipation to maintain relatively stable normal body temperature. In a normal person, axillary temperature fluctuates between 36～37.4℃, and rectal temperature between 36.9～37.9℃.
Body Temperature Regulation
In a normal human body, the processes of heat production and dissipation maintain a relative balance to keep body temperature relatively stable.
1. Body Temperature Regulation Methods(1) Heat Production: The human body's heat production mainly comes from the oxidative metabolic process in the body, and exercise and shivering can also generate heat. When the ambient temperature is around 28℃, at rest, the human body's heat production mainly comes from basal metabolism, with a heat production of 210～252kj/(h·m). During strenuous exercise, heat production increases by 2520～3780kJ/(h·m) or 600～900kcal/(h·m). During exercise, muscle heat production accounts for 90%.
(2) Heat Dissipation: When body temperature rises, the autonomic nervous system regulates skin vasodilation, increasing blood flow by about 20 times the normal amount, and profuse sweating promotes heat dissipation. Profuse sweating in turn causes water and salt loss. Heat exchange between the human body and the environment occurs through the following methods: ① Radiation (radiation): accounts for about 60% of heat dissipation. When the room temperature is 15～25℃, radiation is the main way for the human body to dissipate heat. ② Evaporation: accounts for about 25% of heat dissipation. In a high-temperature environment, evaporation is the main way for the human body to dissipate heat. Evaporating 1L of sweat dissipates 2436kJ (580kcal) of heat. When the humidity is greater than 75%, evaporation decreases. When the relative humidity reaches 90%～95%, evaporation stops completely. ③ Convection: accounts for about 12% of heat dissipation. The rate of heat dissipation depends on the temperature difference between the skin and the environment and the air flow rate. ④ Conduction: accounts for about 3% of heat dissipation. If the human skin is in direct contact with water, because water has a stronger thermal conductivity than air, the rate of heat dissipation is 20～30 times the normal rate.
2. Adaptation to High-Temperature Environment After working in a high-temperature environment for 7～14 days, the human body's ability to adapt to heat stress is enhanced, and it has compensatory capacity against high temperatures, manifested by increased cardiac output and sweating, and lower sodium content in sweat compared to normal people. After full adaptation, the heat dissipation from sweating is twice the normal amount. Those without this adaptive compensatory capacity are prone to heatstroke.
Effects of High-Temperature Environment on Various Body Systems
The damage from heatstroke is mainly due to the direct damaging effect of excessively high body temperature (>42℃) on cells, causing enzyme denaturation, mitochondrial dysfunction, loss of cell membrane stability, and interruption of aerobic metabolic pathways, leading to multiple organ dysfunction or failure.
1. Central Nervous System High heat can cause rapid death of brain and spinal cord cells, followed by focal cerebral hemorrhage, edema, increased intracranial pressure, and coma. Purkinje cells in the cerebellum are extremely sensitive to high heat and often develop dysarthria, ataxia, and dysmetria.
2. Cardiovascular System In the early stage of heatstroke, skin vasodilation causes redistribution of blood, while cardiac output increases, increasing the load on the heart. In addition, persistent high temperatures can cause myocardial ischemia and necrosis, triggering arrhythmias, cardiac dysfunction or heart failure, which in turn leads to a decrease in cardiac output and skin blood flow, further affecting heat dissipation, forming a vicious cycle.
3. Respiratory System During high heat, the respiratory rate and ventilation increase. If it persists and does not relieve, it can lead to respiratory alkalosis. In heatstroke, it can cause damage to pulmonary vascular endothelium and lead to ARDS.
4. Water and Electrolyte Metabolism The maximum sweating rate for a normal person is 1.5L/h. The sweating rate of an individual after heat adaptation is twice that of a normal person. Profuse sweating often leads to water and sodium loss, causing dehydration and electrolyte imbalance.
5. Kidneys Due to severe dehydration, cardiovascular dysfunction, and rhabdomyolysis, acute renal failure can occur.
6. Digestive System The direct thermal injury and reduced gastrointestinal blood perfusion during heatstroke can cause ischemic ulcers, which are prone to massive gastrointestinal bleeding. In patients with heatstroke, varying degrees of hepatic necrosis and cholestasis are present almost 2～3 days after onset.
7. Hematological System In patients with severe heatstroke, varying degrees of DIC can appear 2～3 days after onset. DIC can further promote dysfunction or failure of important organs (heart, liver, kidney).
8. Muscular System In patients with exertional heatstroke, due to increased local muscle temperature, hypoxia, and metabolic acidosis, severe muscle injury often occurs, causing rhabdomyolysis and elevated serum creatine kinase.
Pathology
Autopsy of patients who died from heatstroke reveals necrosis of nerve cells in the cerebellum and cerebral cortex, with Purkinje cell lesions being particularly prominent. The heart shows focal hemorrhage, necrosis, and dissolution of myocardial cells, and hemorrhage in epicardium, endocardium, and valve tissues; varying degrees of hepatic cell necrosis and cholestasis; hemorrhage in the adrenal cortex. Pathological examination after death from exertional heatstroke can reveal degeneration and necrosis of muscle tissue.
Pathophysiology
Heat stress induces thermoregulation and heat acclimatization, acute phase response, and heat shock response that induces the production of heat shock proteins. When heat stress exceeds the body's compensatory capacity, central venous pressure decreases significantly while body temperature rises significantly, leading to thermoregulatory failure, which in turn causes circulatory failure, and increased inflammatory factors (tumor necrosis factor TNF-α, interleukin IL-11 and IL-6) causing endotoxemia further aggravates the circulatory failure. These changes further activate endothelial cells and release vasoactive factors such as nitric oxide and endothelin. The interaction between pyrogenic cytokines, vasoactive endothelial factors, and intracellular ion imbalance leads to a vicious cycle, manifested as high body temperature and central nervous system abnormalities. High body temperature and circulatory failure can cause liver and kidney dysfunction and coagulation disorders. In addition, aging, lack of heat acclimatization, and genetic polymorphism can cause low expression of heat shock proteins and a weakened heat shock response during heat injury, enhancing oxidative damage. Therefore, thermoregulatory failure, excessive acute phase response, oxidative damage, and changes in HSP expression may promote the development of heat stress into heatstroke.
Heatstroke-Clinical Manifestations: Heatstroke can be classified as heat cramps, heat exhaustion, and heatstroke.
Heat Cramps
Often occurs after strenuous exercise in a high-temperature environment with profuse sweating. Muscle spasms often occur after stopping activity, mainly involving skeletal muscles, lasting for a few minutes before relief, with no significant increase in body temperature. Muscle spasms may be related to severe sodium depletion (profuse sweating and drinking hypotonic fluids) and hyperventilation. Heat cramps can also be an early manifestation of heatstroke.
Heat Exhaustion
Often occurs in the elderly, children, and patients with chronic diseases. It is caused by insufficient circulating volume due to excessive loss of body fluid and sodium during severe heat stress. It is characterized by profuse sweating, fatigue, weakness, dizziness, headache, nausea, vomiting, and muscle spasms, with obvious signs of dehydration: tachycardia, orthostatic hypotension, or syncope. Body temperature is mildly elevated without obvious signs of central nervous system injury. Depending on the severity of the condition, examination may show increased hematocrit, hypernatremia, mild azotemia, and abnormal liver function. Heat exhaustion can be an intermediate process between heat cramps and heatstroke. If not treated in time, it can progress to heatstroke.
Heatstroke
A fatal emergency, mainly characterized by high fever (rectal temperature ≥41℃) and disturbance of consciousness. The earliest affected organs are the brain, liver, kidney, and heart. According to the patient's condition and pathogenesis at the time of onset, it is clinically classified into two types: exertional and non-exertional (or classic) heatstroke. Exertional heatstroke is mainly caused by excessive endogenous heat production in a high-temperature environment; non-exertional heatstroke is mainly caused by reduced heat dissipation due to thermoregulatory dysfunction in a high-temperature environment.
1. Exertional Heatstroke: Often occurs during heavy physical labor or strenuous sports in hot, humid, and windless weather. Patients are usually healthy young people who develop the condition several hours after engaging in heavy physical labor or strenuous exercise. About 50% of patients have profuse sweating, and heart rate can reach 160～180 beats per minute with increased pulse pressure. These patients may develop rhabdomyolysis, acute renal failure, hepatic failure, DIC, or multiple organ failure, with a high mortality rate.
2. Non-exertional Heatstroke: Occurs in a high-temperature environment, mostly in elderly and frail urban residents living in crowded and poorly ventilated conditions. Other high-risk groups include patients with schizophrenia, Parkinson's disease, chronic alcoholism, and hemiplegia or paraplegia. It is characterized by dry and hot skin, with 84%～100% of cases having no sweating. Rectal temperature is often above 41℃, with a maximum of up to 46.5℃. The initial manifestations are abnormal behavior or seizures, followed by delirium, coma, and symmetric pupil constriction. In severe cases, hypotension, shock, arrhythmias and heart failure, pulmonary edema, and cerebral edema may occur. About 5% of cases develop acute renal failure, with mild to moderate DIC, and death often occurs around 24 hours after onset.