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Heat Stroke: A Scientific Update

Updated on September 21, 2017
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Ashish has been an intensivist for the past ten years. His areas of interest include hemodyamics and antibiotic stewardship.

Definition

Hyperthermia is the elevation of the core body temperature due to the failure of thermoregulation.

Causes of hyperthermia

The four major hyperthermic syndromes are -

  • Heat stroke
  • Neuroleptic malignant syndrome
  • Malignant hyperthermia
  • Drug-Induced

We will limit our discussion to heat stroke in this article as all four syndromes have a somewhat similar pathogenesis, clinical presentation, sequel and methods of treatment. The prevention and the treatment for heat stroke, the causes, the long-term effects, the recovery and possible complications will be discussed in detail.

Pathophysiology of heat stroke

The body temperature is regulated by keeping a balance between heat production and heat loss. This normal physiology of body temperature regulation determines the pathophysiology of stroke. Even in healthy individuals involved in the normal physical activity, some diurnal variation of temperature is seen. The temperature range of oral temperature is 36.60°C ± 0.38°C. This diurnal variation may produce the highest temperature in this normal range at about 6 pm. The basic understanding of this mechanism guides the treatment for heat stroke.

Mechanisms of heat loss by the body

Heat exchange follows the laws of physics and occurs across a heat gradient. So in a cold environment, the body loses heat to the environment and the vice versa occurs in hot weather.

Evaporation is the main mechanism of heat loss in a hot environment, but this becomes ineffective in a humid climate.

Other methods of heat loss –

  • Radiation
  • Conduction
  • Convection

These methods can only transfer heat across a temperature gradient so hot environment causes heat gain and prevents heat loss.

Levels of hyperthermia

There are three levels of hyperthermia

1) Heat cramps - Painful muscle spasms/cramps usually in legs, arms or abdomen.

2) Heat exhaustion - When no action is taken when a cramp becomes evident.

3) Heat stroke - Can cause impaired mental function, leading to unconsciousness and death.

Heat stroke

Heat stroke is characterized by the following criteria -.

Criteria -

  • Temperature more than 40° degrees centigrade.
  • Depressed mental status or coma.
  • Elevated creatinine kinase level.
  • History of environmental exposure to hot weather.

Types of Heat Stroke

Classic (non-exertional) heat stroke

People with some impairment of thermoregulatory control due to the presence of an underlying disease are affected almost exclusively during a heat wave because their temperature rises easily if a thermal challenge is provided by the environment.


Exertional heat stroke

It occurs in young individuals with intact thermoregulation but it is overwhelmed by the heat production during exertion and the inability of the body to dissipate this heat as high environmental temperature prevents heat dissipation.


Comparison of Classic and Exertional Heatstroke

 
Classic
Exertional
Age
Elderly
Young
Epidemiology
Epidemic (during heat wave)
Sporadic
Predisposing Disease
Present
Absent
Sweating
Absent
Present
Acid Base Disturbance
Respiratory Alkalosis
Metabolic Acidosis
Renal Failure
Uncommon
Common
Rhabdomyolysis
Uncommon
Common
Disseminated Intravascular Coagulation
Uncommon
Common
Hyperuricemia
Mild
Marked
Heat stroke types

Acclimatization in heat stroke

Acclimatization greatly increases heat tolerance by increasing cardiac output and stroke volume.The threshold to start sweating is lower in acclimatized individuals.There is an increase in the volume of sweat via an increase in aldosterone. There is some expansion in the extracellular volume and sodium loss in sweat is minimized.

However, non acclimatized individuals who do not have these adaptive increases in cardiovascular and sweating efficiency clearly have an increased chance of suffering exertional heat stroke.

Heart disease patients are prone to heat stroke.

Mortality is higher in diabetes mellitus, chronic obstructive pulmonary disease and obesity (but it is equivocal whether these conditions make the individual more prone to heat stroke).

Pathogenesis of heat stroke

The main mechanism is an imbalance between heat production and heat loss by the body. Exertion may produce 300-900 kcal/hour and only 500-600 kcal/hour may be lost by sweating. Heat loss due to evaporation is suppressed by impermeable clothing which should never be used in very hot weather.

Other pathological factors which may predispose individuals to heat stroke -

Low potassium levels may cause reduced cardiovascular performance with less blood flow to muscles and skin and heat movement from the body core to the environment is reduced. Diuretics may cause both dehydration and low potassium. Beta blockers also cause cardio depression. Alcohol increases the risk fifteen folds due to the dehydration it causes, by the inhibition of antidiuretic hormone and subsequent diuresis. Dehydration causes decreased skin & muscle blood flow which reduces heat dissipation from the body core to the periphery. This increases the risk of heat stroke.

Oxidative phosphorylation stops at temperatures > 42°C.This temperature is known as the Critical Thermal Maximum as above this limit direct thermal injury to the cells takes place.

Effects of heat stroke on various organs

Central Nervous System

Early stages of heat stroke hypothalamic regulation of body temperature may be in intact but it is lost in later stages. There is direct thermal toxicity to the brain and spinal cord. It may cause cell death, cerebral edema, and hemorrhage. Stupor or coma is universal to heat stroke. Seizures secondary to cerebral edema or hemorrhage may occur. Purkinje cells in the cerebellum are prone to hyperthermia so ataxia, dysmetria, and dysarthria may be present. Cerebrospinal Fluid (CSF) examination may show an increase in protein and slight lymphocytic pleocytosis.

Neurological features are the cardinal features of heat stroke. Delirium, lethargy, coma, and seizures may be present. There can be a permanent neurological injury in about 33 percent patients.

Musculoskeletal System

A rise in temperature causes degeneration and necrosis of muscles due to direct thermal injury. There is more muscle injury in exertional heat stroke due to more local heat, hypoxia and metabolic acidosis due to the exertion involved.

Kidney and Electrolytes

There is a rise in potassium levels due to direct cell injury. Electrolytes are lost through sweat so the total body sodium is reduced. There is reduced phosphate which may be due to parathyroid hormone (PTH) resistance and reduced calcium level due to the intracellular precipitation of calcium in the first two or three days of the disease. Later there is an increase in calcium level due to parathyroid hormone(PTH) activation (2-3 weeks).

The injured cells leak phosphate and calcium causing hypercalcemia and hyperphosphatemia. Hypokalaemia is seen early secondary to heat-induced hyperventilation leading to respiratory alkalosis. Sweat and renal losses may also contribute to hypokalemia. Hyperkalaemia is seen later due to potassium losses from damaged cells and renal failure. Hyperuricemia develops secondary to the release of purines from injured muscle.

Acute renal failure in approximately thirty percent cases. There is a direct thermal injury to kidneys. Pre-renal insult due to volume depletion and renal hypoperfusion. Rhabdomyolysis may also cause renal injury.

Gastrointestinal System

The combination of direct thermal injury and hypoperfusion of the intestines frequently leads to ischemic intestinal ulceration that may result in frank bleeding. The liver is very susceptible to injury. It is affected in every case. Hepatic necrosis and cholestasis by second or third day. In five to ten percent of patients, liver injury may be the cause of death.

Hematological System

There is an increase in white blood cell (WBC) count due to catecholamine release & hemoconcentration. Bleeding may occur due to the direct activation platelets and coagulation factors. There is a reduction in coagulation factors due to liver failure. There is an unexplained reduction in platelet count.

Vascular endothelial heat injury initiates a coagulation cascade triggered which may cause Disseminated Intravascular Coagulation (DIC) on the second or third day. DIC is present in all fatal cases. There is Increased blood viscosity in 24% cases and it facilitates thrombus.

Endocrine

There is hyperglycemia due to increased cortisol secretion. Later hypoglycemia may follow due to the exhaustion involved. Adrenal cortical hemorrhage may be present. There may be some adrenal dysfunction in patients.

Pulmonary

There is vascular endothelial damage in the lungs. It may present with cor pulmonale or ARDS. Some myocardial dysfunction is always present so pulmonary edema is common. There may be acid-base abnormalities in the form of respiratory acidosis and metabolic alkalosis.


Assessment

Consider heat stroke in the differential diagnosis of patients with altered mental state and exposure to heat.

  • The classic triad of hyperthermia, neurological abnormalities, plus dry skin.
  • Measure temperature with a rectal or esophageal probe.
  • Sweating can still be present.
  • Hypotension and shock 25% patients.
  • Hypovolaemia, peripheral vasodilatation and cardiac dysfunction.
  • Sinus tachycardia.
  • Hyperventilation is a universal finding in heat stroke.

Investigations

  • Hypokalemia.
  • Hyperphosphatemia and hypercalcemia.
  • Hyperkalemia may be present if rhabdomyolysis has occurred.
  • Renal impairment.
  • Urate is frequently high and may play a role in the development of acute renal failure.
  • Glucose is elevated in up to 70% of patients.
  • Liver function tests are almost always deranged in exertional heat stroke.
  • Transaminase and lactate dehydrogenase most commonly elevated.
  • Creatine kinase is between 10000 to 1000000 in rhabdomyolysis.
  • White cell count is as high as 30,000 to 40,000.
  • Coagulation tests are routinely abnormal and disseminated intravascular coagulation may occur.
  • Lactic acidosis may be present.
  • Compensatory respiratory alkalosis.
  • Serum or urine myoglobin may be elevated.

ECG and X-Ray

ECG- Rhythm disturbances like sinus tachycardia, supraventricular tachycardia (SVT) or Atrial Fibrillation (AF).

Conduction defects- RBBB(right bundle branch block) and intraventricular conduction defects.

QT prolongation (most common secondary to low potassium, calcium, magnesium)

ST changes (secondary to myocardial ischemia).

Chest X-Ray may show ARDS or aspiration.

Management of Heat Stroke

Cooling Methods

  • The mainstay of therapy and must be initiated from the onset.
  • Use of cooling methods in pre-hospital period may be life-saving.
  • Initially, remove the patient from the heat source and remove all clothing.
  • Evaporative cooling – tepid water on the skin with fans.
  • Ice water immersion – most effective method but practically difficult and cannot be used with monitors and other equipment and uncomfortable for the patient.

Cooling methods

Emergency cooling method used for the treatment of heat stroke
Emergency cooling method used for the treatment of heat stroke | Source

Cooling Methods: The Most Important Treatment for Heat Stroke

Ice packs to axilla, groin, and neck.

Cooling blankets and wet towels.

Peritoneal lavage can be considered in severe resistant cases.

Shivering may occur in rapid cooling – this will increase oxygen consumption and heat production.

Sedate.

Paralyze.

Paracetamol and aspirin are ineffective and should not be used.

Stroke Protocol: ABC management

A

  • Endotracheal tube if needed. Consider early intubation. Avoid suxamethonium for intubation.

B

  • Monitor respiratory rate and oxygen saturation.
  • Look for evidence of aspiration.
  • Ventilate as per lung injury protocol.

C

  • The patient may have a large fluid deficit.
  • Normal saline is probably best (avoid lactate and potassium containing fluids).
  • Monitor heart rate, blood pressure, and urine output.
  • Vasopressors may be needed but adrenergic agents can impair heat dissipation by causing peripheral vasoconstriction.

If prompt effective treatment not undertaken mortality approaches 80%.

Mortality should be less than 10% with prompt treatment.

Peak temperature and time spent at elevated .temperature are most important prognostic factors.

Heat exchangers, therefore, have a very important role in the treatment for heat stroke

The Others

Heat Cramps

There are painful involuntary spasms of major muscles usually in heavily exercised muscle groups. Dehydration and salt loss also play a role. Rest rehydration and salt replacement are the treatment.

Heat Exhaustion

It is a mild heat stroke. The physiological process involved is the same. Patients can still have the capacity to dissipate heat and the brain activity is not impaired. Volume depletion is still a problem. The basic treatment is the same as the treatment for heat stroke with the same underlying principles.

The other causes of hyperthermia are not due to environmental exposure. These conditions should be considered in the differential diagnosis of heat stroke as the treatment for heat stroke and the other hyperthermic syndromes overlap. These can be discussed in subsequent articles.

Awareness regarding the mortality and morbidity caused by heat stroke is necessary as prevention is always better than cure. The prompt and aggressive treatment for heat stroke is life saving.

Have you ever suffered from some sort of heat injury?

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