Heat Stroke: How To Be Safe From The Killer Of The Summer ?

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What is heat stroke?

Heat stroke is a type of hyperthermia accompanied by a systemic inflammatory response that causes multi-organ dysfunction syndrome with encephalopathy as its primary symptom.

Despite vigorous treatment and proper cooling of the body temperature, heat stroke frequently results in death, and those who do survive may have lifelong brain impairment. According to data from the Centers for Disease Control and Prevention, extreme heat was to blame for 7000 deaths that occurred in the United States between 1979 and 1997. With global warming and the anticipated worldwide increase in the frequency and intensity of heat waves, the incidence of these deaths could rise.

Epidemiology of heat stroke

The incidence of heat stroke during heat waves in American cities ranged from 17.6 to 26.5 incidents per 100,000 people, according to an epidemiologic study. The majority of sufferers of traditional heat stroke are very young or very old, destitute, socially isolated, and without access to air conditioning.

Seasonal variations incidence in Saudi Arabia range from 22 to 250 incidences per 100,000 people. In Saudi Arabia, the crude fatality rate from heat stroke is thought to be 50%.

Saudi Arabia’s prevalence of heat exhaustion, nevertheless, varies from 450 to over 1800 cases

for every 100,000 people. The risk of heat stroke may be influenced by genetic factors; possible susceptibility genes include those that code for cytokines, Involving coagulation proteins and heat-shock proteins in preparing for heat stress

Pathogenesis

1) Thermoregulation

Heat is created by metabolism and is obtained from the environment. The thermoregulation mechanism is necessary to keep the body temperature at 37°C to dissipate this total heat burden. The hypothalamus thermoregulatory center is alerted by peripheral and hypothalamic heat receptors when blood temperature rises by less than 1°C, and the efferent response from this region increases the flow of warm blood to the body’s surface.

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The blood flow in the skin is then increased by up to 8 liters per minute by active sympathetic cutaneous vasodilation. Thermal sweating is also triggered by a rise in blood temperature. Tachycardia, an increase in cardiac output, and an increase in minute breathing are all brought on by a higher blood temperature. 

Visceral perfusion is decreased, notably in the intestines and kidneys, as blood is diverted from the central circulation to the muscles and skin to aid in heat dissipation.  To improve thermoregulation, losses of salt and water from perspiration, which may total 2 liters or more per hour, must be compensated by liberal salt supplementation.

2) Acclimatization

Through gradual increases in the amount of work done in a hot environment, a person gradually develops the adaptations necessary to work safely in temperatures that were once unpleasant or life-threatening.  Acclimatization to heat requires several weeks and involves improving cardiovascular function, activating the renin-angiotensin system, and  Aldosterone axis, sweat glands’ ability to save salt and kidneys, an improvement in secretory ability perspiration, a rise in the plasma volume, and glomerular filtration rate as well as an improvement in resistance to exertional rhabdomyolysis.

Heat Stroke

3) Acute phase response

Endothelial, leukocyte, and epithelial cells work together in the acute-phase response to heat stress to prevent tissue damage and encourage tissue healing. The first recognized mediator of the systemic inflammation brought on by vigorous exercise was interleukin-1. many cytokines

are now recognized to be created in reaction to internal or external heat. Fever, and leukocytosis, are mediated by cytokines.

Activation of leukocytes and endothelial cells, as well as repair and healing of the hypothalamic-pituitary-adrenal axis, are all facilitated by other acute-phase proteins. These proteins also promote endothelial-cell adhesion, proliferation, and angiogenesis.

4) Heat shock reaction

Stress or heat-shock proteins are almost always produced by cells in response to abrupt heating.  Gene transcription primarily regulates the expression of heat-shock proteins. When under heat stress, one or more heat-shock transcription factors bind to the heat-shock element, increasing the rate at which heat-shock proteins are transcribed.  A cell can temporarily tolerate a second, otherwise fatal, stage of heat stress when the amount of heat-shock proteins in the cell is elevated.

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Another potential mechanism involves heat-shock proteins, which control the baroreceptor-reflex response under extreme heat stress by reducing bradycardia and hypotension and providing cardiovascular protection.

Progression from Heat Stress to Heat Stroke

1) Thermoregulatory Failure

An increase in cardiac output of up to 20 liters per minute and a transfer of heated blood from the core circulation to the peripheral circulation are the typical cardiovascular adaptations to extreme heat stress. Increased susceptibility to heat stroke can occur when the body is unable to boost cardiac output due to salt and water loss, cardiovascular disease, or a drug that interferes with cardiac function.

2) Acute-Phase Response Exaggeration

It’s conceivable that the digestive system stimulates the inflammatory response. Ischemia of the gut and intestinal hyperpermeability result from blood shifting from the mesenteric circulation to the working muscles and skin during severe exercise or heat. In animal models, there is ample proof of hyperpermeability during heat stress, but there is far less proof of this phenomenon in people.

3) Alteration of Heat-Shock Response

This adaptive response may be protective because the heat-shock response is lessened during heat stroke. Aging, a lack of acclimation to heat, and specific genetic polymorphisms are examples of conditions linked to low levels of heat-shock protein expression that may favor the transition from heat stress to heat stroke.

Clinical manifestations of heat stroke

These observations are crucial for heat stroke.

  • The core temperature may range from 40°C to 47°C.
  • Inappropriate behavior or impaired judgment.
  • There is a chance of seizures, especially after cooling.
  • Tachycardia and hyperventilation.
  • Carbon dioxide tension is often less than 20 mm Hg.
  • Respiratory alkalosis.
  • Hypophosphatemia and hypokalemia.
  • Rhabdomyolysis, hyperphosphatemia, hypocalcemia, and hyperkalemia.
  • syndrome of many organ dysfunctions includes pancreatitis, encephalopathy, rhabdomyolysis, acute renal failure, acute respiratory distress syndrome, myocardial injury, hepatocellular injury, intestinal ischemia or infarction, and hemorrhagic complications, particularly disseminated intravascular coagulation with pronounced thrombocytopenia.
Heat Stroke
A heat stroke patient in Karachi, Sindh

Treatment of heat stroke

The following strategy is used for the treatment of heat stroke.

Cooling

Therapeutic cooling methods, therefore, try to speed up heat transfer from the skin to the environment while maintaining blood flow to the skin. In practice, cold water or ice is administered to the skin, which is also fanning. most of these techniques reduce the skin’s temperature below 30 degrees Celsius, causing cutaneous vasoconstriction and shivering. There are no pharmacological treatments for heat stroke that speed up cooling.

 Despite being taken into consideration, dantrolene sodium was shown to be unsuccessful in double-blind, randomized research. Despite research showing that pyrogenic cytokines may contribute to heat stress, the effect of antipyretic medications on heat stroke has not been examined. In the majority of patients who receive timely and intensive therapy, recovery of central nervous system function during cooling is a positive prognostic indicator and should be anticipated. About 20% of patients have a residual brain injury, which is linked to a high mortality rate.

Prevention

People can prepare themselves for heat, plan outside activities for cooler times of the day, limit their degree of physical activity, drink more water, eat salty foods, and spend more time indoors where it is air-conditioned to prevent both types of heat stroke. Children should never be left in a hot car unsupervised, and vehicles should always be locked.

A strategy to enhance weather forecasts, warn at-risk individuals, provide easily accessible air-conditioned shelters, and lower energy costs during extreme weather may lessen morbidity and mortality during heat waves.

Conclusion

Heat stroke is becoming more and more likely. Heat waves are already a result of global warming in temperate regions. Research in this area should be prioritized due to the understanding that thermoregulatory failure and impaired control of inflammatory and stress responses enhance the transition from heat stress to heat stroke and increase the severity of tissue injury. A new paradigm of immunomodulation and novel preventive interventions will be suggested by a better understanding of the cellular and molecular reactions to heat stress. This could reduce the multiorgan damage brought on by heat stroke in many people.


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