Defined as a core temperature greater than 40.5°C, with CNS dysfunction including delirium and coma.
Heat stroke is a medical emergency that requires rapid recognition and treatment to prevent permanent complications and death.
Mortality from classic heat stroke approaches 80% and, for exertional heat stroke, 33% in the absence of prompt treatment.
It is the most hazardous condition of illnesses that progressed from heat exhaustion to heatstroke.
Heat accumulation overrides the ability for heat dissipation during exercise or exposure to environmental heat stress.
Characterized by CNS dysfunction, multiorgan failure, and extreme hyperthermia with temperature is usually greater than 40.5°C.
Heat stroke is characterized by the triad of hyperthermia, neurologic abnormalities, and recent exposure to hot weather, physical exertion, or both.
Associated with dry skin, rapid pulse, headache, dizziness, nausea, impaired mentation and unconsciousness.
Tachypnea, tachycardia, and hypotension are common.
Sweating is typical of exertional heat stroke, whereas in cases of classic heat stroke, the skin is often hot and dry.
early manifestations include behavioral changes, confusion, delirium, dizziness, weakness, agitation, combativeness, slurred speech, nausea, and vomiting.
Seizures and incontinence may occur.
Only rectal temperatures are accurate enough to demonstrate hyperthermia.
Most severe manifestation of heat related illness.
Primary pathophysiology involves transitioning from a compensable thermoregulatory phase in which heat loss exceeds heat gain to a non-compensable phase in which heat gain is greater than any loss and when cardiac output is insufficient to cope with the high thermoregulatory needs.
As the body temperature rises, it leads to direct cytotoxic effects and then an inflammatory response that creates multi organ failure.
Elevated body temperatures trigger a stress response that involves endothelial cells, leukocytes, epithelial cells, all of which provide protection against tissue injury and promote cell repair.
The stress reaction is mediated by a family of heat-shock proteins and by changes in plasma and tissue levels of pro inflammatory and anti-inflammatory cytokines.
Hyperthermia that is prolonged causes circulatory failure, hypoxemia, increased metabolic demands, and heat related cytotoxic effects increase, manifesting in the dysregulation of the inflammatory reaction.
Categorized as either passive or exertional
Classically it is due to exposure to environmental heat and poor heat dissipation.
Exertional heatstroke is associated with physical exercise and results with excessive production of metabolic heat overwhelms heat loss mechanisms.
The incidence of exertional heatstroke is unknown but epidemiologic studies suggest steady increase in morbidity and mortality.
Exertional heat stroke can occur even within the first 60 minutes of exertion and may be precipitated without exposure to high ambient temperatures.
Associated with a poor prognosis.
Exertional heat stroke is a medical emergency, which is directly related to strenuous physical activity, and can strike individuals engaging in activities that many performed previously in an uneventful fashion.
Exertional heat stroke occurs most often among healthy young individuals and prompt recognition and treatment results in mortality rates of 5% or less.
It occurs frequently as an epidemic among older individuals whose ability to adjust the heat stress is compromised, in chronically ill persons, and those who cannot care for themselves.
Increased urbanization with inner-city heat islands and rising global temperatures are major extrinsic factors contributing to heatstroke.
Heat exhaustion, refers to a less severe form of heat related disease and is associated with nonspecific symptoms of weakness, malaise, headache and nausea.
Heat waves kill more people, on average, than any other extreme weather events.
Heat exhaustion can progress in some patients to heatstroke.
Older persons are more vulnerable to heat due to their diminished thermoregulatory capacity.
The mortality from heatstroke among the elderly exceeds 50%.
Because of a high ratio of surface area to mass, an underdeveloped thermoregulatory system with small blood volume relative to body size, a low sweating rate, prepubertal children are a population at risk from heatstroke.
Heatstroke related inflammatory response is similar to the systemic inflammatory response syndrome related to sepsis.
Systemic inflammatory response is mediated be circulating messenger RNAs which trigger the release of cytokines and the high mobility group box 1 protein leading to excessive activation of leukocytes and endothelial cells.
Heatstroke is a form of hyperthermia associated with a systemic inflammatory response leading to multi organ dysfunction in which encephalopathy predominates.
Neutrophil activation in heatstroke is a link between inflammatory and coagulation responses.
Heatstroke reduces intestinal blood flow and can cause gastrointestinal ischemia affecting cell viability and cell wall permeability.
This gastrointestinal ischemia results in oxidative and nitrous stress damages of cell membranes opening cell-to-cell junctions, and allowing endotoxins and other pathogens to leak in the systemic circulation, overwhelming the detoxification capacity of the liver and results in endotoxemia.
Diagnosis is mainly a clinical one, based on the triad of hyperthermia, neurological abnormalities, and recent exposure to hot weather or physical exertion.
Patients commonly experienced tachycardia, tachypnea, and hypotension.With exertional heat stroke profuse sweating and wet skin is typical, whereas in classic heat stroke the skin is usually dry.
Dry skin in classic heat stroke, reflects the decreased sweat-gland response and output in elderly people under heat stress.
The skin with heatstroke may be flushed, reflecting excessive vasodilation, or pale indicating the presence of vascular collapse.
Death can occur within a few hours in infants during hot weather when confined in a closed car.
Overmotivation, peer pressure, alcohol and drug abuse are risk factor for exertional heatstroke.
Heat stroke is managed with acute resuscitation measures followed by rapid cooling, reducing the core body temperature to 38 to 39°C, ideally within 30 minutes after presentation.
For exertional heatstroke management by a cooling rate faster than 0.10°C per minute is safe and desirable to improve the prognosis.