What Is The Treatment For Heat Stroke: An Update
Hyperthermia is the elevation of core body temperature due to 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 of heat stroke, the causes, the long term effects, the recovery and possible complications will be discussed in detail.
Physiology of Temperature regulation
The body temperature is regulated by keeping a balance between heat production and heat loss.Even in healthy individuals involved in 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.
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 –
These methods can only transfer heat across a temperature gradient so hot environment causes heat gain and prevents heat loss.
How does the body loose heat?
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 cell takes place.
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 is characterized by the following criteria -.
- Temp more than 40 degree celsius.
- 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 on a thermal challenge 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 inability of the body to dissipate this heat as high environmental temperature provides a unfavourable gradient for heat dissipation .
Comparison of Classic and Exertional Heatstroke
Epidemic(During heat wave)
Acid Base Disturbance
Disseminated Intravascular Coagulation
Pathogenesis of heat stroke
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 body core to 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 anti diuretic hormone and subsequent diuresis.
Dehydration→ Decreased skin & muscle blood flow →Heat dissipation from the body core to periphery is reduced and risk of heat stroke increases greatly.
Non acclimatized individuals are more prone to 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 increased volume of sweat via an increase in aldosterone. There is some expansion in the extracellular volume and sodium loss in sweat is minimised. .
However,unacclimatized 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 higher in Diabetes Mellitus,Chronic Obstructive Pulmonary Disease and Obesity (but its equivocal whether these conditions make the individual more prone to heat stroke).
Central Nervous System Manifestations
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 oedema and haemorrhage.Stupor or coma is universal to hyperthermic syndromes. Seizures secondary to cerebral oedema or haemorrhage 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 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 permanent neurological injury in about thirty three percent patients.
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 the the exertion involved.
Rise in Potassium level due to the cell injury.
Electrolytes are lost by sweat so the total body sodium is reduced.
Reduced phosphate - Parathyroid hormone (PTH)resistance
- Intracellular tapping.
Reduced Calcium level – Intracellular precipitation (2-3 days).
Increse in Calcium Level- Parathyroid Hormone(PTH) activation (2-3 weeks).
Injured cells leak phosphate and calcium causing hypercalcaemia and hyperphosphataemia.
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.
Hyperuricaemia develops secondary to the release of purines from injured muscle.
Acute renal failure in approximately thirty percent cases.
Direct thermal injury to kidneys.
Pre-renal insult due to volume depletion and renal hypoperfusion.
Rhabdomyolysis may also cause renal injury.
The combination of direct thermal injury and hypoperfusion of the intestines frequently leads to ischemic intestinal ulcerations that may result in frank bleeding.
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.
Increase in White Blood Cell(WBC)count due to catecholamine release & haemoconcentration.
Bleeding may occur due to the direct activation platelets and coagulation factors.There is reduction in coagulation factors due liver failure.Unexplained reduction in platelets.
Vascular endothelial heat injury– coagulation cascade triggered.
Disseminated Intravascular Coagulation on second or third day.
Present in all fatal cases.
Increased blood viscosity (24%) facilitates thrombus.
Hyperglycaemia due to increased cortisol.
Later hypoglycaemia may follow due to exhaustion.
Adrenal cortical haemorrhage may be present.
Little evidence of adrenal dysfunction also there.
Vascular endothelial damage
Some myocardial dysfunction—So pulmonary edema common
Respiratory alkalosis+ Metabolic acidosis.
Consider heat stroke in the differential diagnosis of patients with altered mental state and exposure to heat.
- Classic triad of hyperthermia, neurological abnormalities and dry skin.
- Measure temperature with rectal or oesophageal 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.
- Hyperphosphataemia and hypercalcaemia.
- Hyperkalaemia may be present if rhabdomyolysis has occurred.
- Renal impairment.
- Urate – Frequently high and may play a role in the development of acute renal failure.
- Glucose – Elevated in up to 70% of patients.
- Liver function tests - Almost always deranged in exertional heat stroke.
- Transaminase and lactate dehydrogenase most commonly elevated.
- Creatine kinase– 10000 to 1000000 in rhabdomyolysis.
- White cell count is as high as 30,000 -40,000.
- Coagultion tests – Routinely abnormal and disseminated intravascular coagulation may occur.
- Acid Base– Lactic acidosis may be present.
- Compensatory respiratory alkalosis.
- Myoglobin – Serum or urine myoglobin may be elevated.
ECG and X Ray
ECG –Rhythm disturbances (sinus tachycardia, Supra ventricular Tachycardia (SVT)or Atrial Fibrillation (AF).
Conduction defects - RBBB(right bundle branch block) and intra ventricular conduction defects.
QT prolongation (most common secondary to low Potassium , Calcium and Magnesium)
ST changes (secondary to myocardial ischemia).
Chest X Ray may show ARDS or aspiration.
Management of Heat Stroke
- Mainstay of therapy and must be initiated from the onset.
- Use of cooling methods in pre hospital period may be life saving.
- Initially remove patient from 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.
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.
Paracetamol and aspirin are ineffective and should not be used.
- Endotracheal tube if needed.Consider early intubation.Avoid suxamaethonium for intubation.
- Monitor Respiratory Rate and oxygen saturation.
- Look for evidence of aspiration .
- Ventilate as per lung injury protocol .
- Patient may have a large fluid deficit.
- Normal saline is probably best ( lactate and avoid 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 exhaustion – mild heat stroke.
Same physiological process.
Patients can still have the capacity to dissipate heat and the brain activity is not impaired.
Volume depletion is still a problem.
Painful involuntary spasms of major muscles
Usually in heavily exercised muscle groups
Dehydration and salt loss also thought to play a role
Rest rehydrate and replace salts
The other causes of hyperthermia are not due to environmental exposure.These conditions should be considered in the differential diagnosis of hyperthermia and are mentioned in the beginning.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.