Heat stroke

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.

There are three phases to the process, which are seen more clearly in exertional heat stroke then in classic heat stroke: a hyperthermic-neurologic acute phase, a hematologic-enzymatic phase which peaks 24-48 hours after the event, and a late renal-hepatic phase if clinical symptoms are sustained for 96 hours or longer.
Some cases of neurologic damage with cerebellar ataxia, dysarthria, cognitive disorders, and anti-retrograde amnesia made persist  for several weeks to months.
Following heat stroke the risk of death after recovery may be higher than the risk for the general population.
Most critical is recognition of the acute phase, since prompt recognition and treatment may be life-saving.

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.

Any systemic disease with a similar clinical picture of fever and manifestations of brain dysfunction should be considered only after heat stroke has been ruled out.
The brain has extreme sensitivity to hyperthermia so that CNS disturbances are inevitable with heat stroke.
Early CNS symptoms include behavioral changes, confusion, delirium, dizziness, weakness, agitation, slurred speech, nausea, combativeness, and vomiting.
While consciousness deteriorates commonly, it usually improves once the temperature falls below the critical level of 40.5°C.
The brain injury appears to be related to edema. which is most concentrated in the cerebellum, with generalized atrophy and evidence of involvement of the Purkinje cell layer.
Heat stroke related neuronal injury to the autonomic and enteric nervous systems may be prolonged.
Damage to the anterior hypothalamus may be responsible for the loss of thermal regulation.
Patients may experience seizures and sphincter incontinence in severe cases of, exertional heat stroke.
Multi organ system failure is more pronounced in exertional heat stroke than in classic heat stroke and may peak within 24-48 hours.
With prompt treatment clinical signs abate in most cases within a few days, most patients recover without lasting effects.
Sustained heat stroke may result in alteration in consciousness, DIC, acute respiratory distress syndrome, acute renal, cardiac, and hepatic dysfunction with failure..
Rhabdo holy sis is typical with exertional heat stroke.
Differential diagnosis include: meningitis, encephalitis, epilepsy, drug intoxication, severe dehydration, and any metabolic syndrome.
Any delay in the treatment of heat stroke substantially increases morbidity and mortality.
The primary management is the alleviation of hypothermia.
Prognosis worsens if the core body temperature is steamed above the threshold of 40.5°C.
Rapid and affective cooling is the corner stone of treatment and is delayed only for cardio pulmonary resuscitation.
A target temperature below 39°C lessens to the risk of clinical deterioration.
Autopsy studies show that end organ failure following heat stroke is due to heat induced necrotic and apoptotic cell death accompanying microthrombosis , hemorrhage, and inflammatory injury.

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.

The immersion in cold water for the treatment of exertional heatstroke can achieve a cooling rate of 0.2° to 0.5°C per minute is the acceptable treatment  of choice.
Where ice is not available a cooling rate of approximately 0.10°C per minute can be achieved by pouring copious amounts of water over the body.
In the elderly with classic heat stroke cold water immersion has acceptable cooling rate associated with it, but the treatment of choice involves conductive or evaporative cooling, such as ice packs, cold packs, or wet cause sheets, and fanning: these methods are less efficient than cold water immersion for a better tolerated in the elderly.
The most effective cooling methods are cold water immersion and ice water immersion, with no difference in cooling rates between these messages.
No pharmacologic agents accelerate cooling.
Antipyretic agents such as aspirin and acetaminophen are ineffective in heat stroke, since the fever and hyperthermia  raise the core body temperature through different physiological pathways.
Antipyretic agents aggravate coagulopathy and liver injury with heat stroke.
Prompt cooling in most cases rapidly reversed heat Induced organ dysfunction.
A rapid rate of cooling, ideally 0.2° to 0.5°C per minute with continuous monitoring of core temperature is safe and associated with a better prognosis than slower cooling.
Cooling measures should be undertaken before and during transport to a hospital, if possible.
Patients who are successfully cooled and survive the hyperthermic-neurologic phase are at higher risk of progression to a hematologic enzymatic in late hepatic renal phases.

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