HEAT Stroke

INTRODUCTION 

The current heat wave condition triggered by the El Nino Phenomenon , name given to above-normal temperatures in the Pacific Ocean that have the potential to cause devastating conditions around the world especially for the tropical country , and Malaysian being in the equatorial climate poses significant risk of heat injuries for all individuals especially for those participating in strenuousphysical activities as in endurance sports, military training and working outdoors (eg. construction workers). 

PATHOPHYSIOLOGY

                                 

The classical models of heat stroke attributed the pathogenesis of heat stroke to the direct cytotoxic effect of hyperthermia coupled with circulatory shock resulting from excessive dehydration. Hyperthermia results in internal organ tissue temperatures rising above critical levels causing damage to the cell membranes and energy systems. Dehydration and salt depletion impairs thermoregulation and the compromise in blood circulation reduces blood flow to the major organs, causing them to fail

eventually. However, these factors cannot explain fully the observation of systemic coagulation, massive haemorrhages and other sepsis-like clinical symptoms observed in heat stroke

patients.

Recent models of heat stroke suggest that heat stroke may be triggered by the coupling of hyperthermia and endotoxemia.

Endotoxins or lipopolysaccharides (LPS) play an important role in fuelling the inflammatory response. Under resting conditions,the epithelium of the intestinal wall forms the barrier that prevents

LPS from infiltrating the sterile environment of the circulating blood. However, the integrity of the gut epithelium is compromised during exercise and heat stress, resulting in the

translocation of LPS into the blood circulation system.Mild endotoxemia has been reported in endurance athletes during races and in laboratory settings. This is also observed at moderate heat stress levels. 

The body, under normal circumstances, clears circulating LPS the recticuloendothelial system of the liver, high density lipoproteins and LPS antibodies.A period of intense exercise may compromise the anti-LPS system, thus impairing the removal of LPS and hence reduce heat tolerance. Similarly, in immunecompromised individuals, where LPS clearance is suppressed, endotoxemia can develop and LPS can accumulate to a concentration that triggers sepsis, which in turn, triggers the systemic inflammatory response. Sepsis and systemic inflammation results in disseminated intravascular coagulation, central nervous system dysfunction and multi-organ failure. 

TYPES OF HEAT INJURIES

1. Mild Heat-Related Illness

A. Heat Syncope 

Occurs with orthostatic hypotension resulting from volume depletion, peripheral vasodilatation (physiologic response to heat production) and venous pooling. Prolonged standing after

significant exertion and rapid change in body position after exertion, such as from sitting to standing, may lead to heat syncope. 

B. Heat Cramps

Acute, painful and involuntary muscle contractions that occur during or after intense exercise sessions in the heat. Muscles involved are usually the calf, quadriceps and abdominal muscles. Heat cramps are associated with fluid deficiencies (dehydration), electrolyte imbalances and neuromuscular fatigue. They are one of the earliest indications of heat injuries and may occur independently or with other symptoms of heat exhaustion.

C. Heat Rash

Blocked eccrine sweat glands.

2.  Heat Exhaustion

Exhaustion is a physiologic response to work defined as the inability to continue exercise.

Heat exhaustion is characterised as follows:

1. Inability to continue strenuous physical exertion due to fatigue from heat stress.

2. Normal mental state and stable neurological status.

Heat exhaustion may be associated with mild central nervous system (CNS) or other non-specific symptoms such as profuse sweating, nausea, vomiting, headache, dizziness, lightheadedness, intestinal cramps, weakness, hyperventilation and cool and clammy skin. The core temperature is usually in the range of 37.7o C to 40o C. 

If heat exhaustion is not treated appropriately, it can progress to heat stroke.  

3. Heat stroke

Heat stroke is a serious and potentially fatal systemic condition that occurs when the thermoregulation system is overwhelmed. It is a form of hyperthermia associated with a systemic inflammatory response leading to a syndrome of multi-organ dysfunction in which encephalopathy predominates. 

Heat stroke can be categorized into :  

A. Exertional Heat Stroke
B. Non Exertional (Classical )

A. Exertional heat stroke occurs during physical exertion, when hyperthermia is due largely to the inability to remove endogenous metabolic heat. Athletes, outdoor adventure enthusiasts,

military personnel and manual workers who work under hot and humid conditions are exposed to the risk of exertional heat stroke.

B. Non Exertional (Classical ) heat stroke occurs during passive exposure to environmental heat stress.It is most frequently observed during heat waves. Young children, the aged sick,schizophrenic

patients and patients who are bed-ridden are particularly vulnerable to classical heat stroke during heat waves. In aged patients, existing chronic illnesses (e.g. heart disease) may contribute to the higher morbidity and mortality from heat stroke in extremely hot weather.  Classical heat stroke has been attributed to impairment of homeostatic mechanisms under conditions of high ambient temperature. 

                                   

PREVENTION OF HEAT INJURIES

1. Screening

There are currently no tests to effectively screen individuals for their risk of heat injury. 

2. Education

Individuals should be educated to balance their fluid intake with sweat and urine losses to maintain adequate hydration status.Adequate rest and a balanced diet prior to strenuous physical activity may be beneficial.

3. Heat acclimatisation

The heat acclimatisation process involves 10 to 14 days of gradual increase in duration of exposure to performing moderate work under hot weather conditions. Physiological adaptation can be observed from the 4th day and are usually optimised by 10 to 14 days. 

4.Hydration

Appropriate hydration is important to minimize health risks. One should start the exercise activity in a euhydrated state. During the activity, it is normal to be slightly dehydrated, but the degree of

dehydration should not exceed 2% of body weight. After the activity the athlete should continue drinking fluid at regular intervals to correct the fluid deficit incurred during the activity. If time permits, consuming normal meals and beverages will restore euhydration. 

5. Minimize barriers to evaporation

While exercising in hot and humid conditions, minimise the amount of clothing and equipment as these may retard heat loss from evaporation. 

6. Work-rest cycle

Exercise intensity and environmental conditions should be the main determinants in deciding the duration of physical activity and frequency of rest breaks.

MANAGEMENT OF HEAT STROKE

The following measures should be instituted in the management of heat exhaustion and heat stroke :

         

1. General Measures

1.Transfer the patient to a cooler and shaded environment.

2. Assess the patient's airway, breathing and circulation (ABCs) and institute basic resuscitative support as appropriate.

3. Measure core body temperature with a rectal thermometer

4. Institute immediate and aggressive cooling efforts to reduce core body temperature. 

5. Maintain hemodynamic stability. Individuals who do not improve rapidly should be transported

to an emergency department. Progressive worsening of consciousness should trigger a detailed evaluation for hyperthermia, hyponatraemia, hypoglycaemia and other medical problems.

2. Specific Measures 

Morbidity and mortality are directly related to the duration and intensity of elevated core body temperature.Treatment protocols for heat injuries thus aims to lower the core body temperature to an acceptable level as rapidly as possible. Early diagnosis and proper treatment are critical for the patient's survival. 

A. Treatment of heat cramps

To relieve muscle spasms, the individual should stop the activity and initiate mild stretching and massage the muscle. Recumbent position may allow more rapid distribution of blood

flow to cramping leg muscles. Sodium-containing sports beverage may prevent or relieve

cramping in athletes who lose large amounts of sodium in their. Intravenous hydration with 0.9% normal saline may be required in severe or refractory cases when the symptoms

continue to rebound. 

B. Treatment of heat syncope

To treat heat syncope, rest in a cool place and in a supine position with both legs and hip elevated to increase venous return.. Other causes of syncope need to be ruled out.

C. Treatment of heat exhaustion and heat stroke

Lowering the core body temperature. Rapid cooling is desirable as decreasing body temperature to

below 39o C within 30 minutes of presentation has been shown to improve survival. 

1. Non-Invasive Cooling Methods

Cooling by ice packs and tap water

Heat Stroke In Karachi , Pakistan.
Source www.independent.co.uk

A simple and efficient method to effect body cooling is to spray copious volumes of tap water directly on the skin and to facilitate evaporation using a fan. Placing ice packs in the axilla, groin and neck has also been recommended to promote body cooling.Cooling by tap water and the application of ice packs can be used as the initial cooling methods prior to evacuating a heat injury patient to a medical facility. 

Cooling by immersion

The optimal method of rapidly cooling patients has been a matter of debate for some time. A 2013 guideline from the Wilderness Medical Society recommends ice-water immersion as a superior method for rapidly lowering core body temperature below the critical levels normally found in heatstroke patients

Immersion of a heat stroke patient in ice water provides effective whole body cooling and reduces morbidity and mortality in exertional heat stroke. The rate of cooling has been reported to be

in the range of 0.15 to 0.24°C/min.Immersion in ice water may be done to manage exertional heat

stroke occurring in young people, military personnel, and athletes. However, this technique was found to be poorly tolerated among the elderly and was associated with increased morbidity and

mortality. Early studies reported severe shivering, agitation, and combativeness in this group, which often required restraining and sedation of the patient.

Cooling by evaporation

Evaporative cooling is based on the physical principle that the conversion of 1.7ml of water to gaseous phase consumes 1kcal of heat Evaporation-based cooling can be achieved by

continuous spraying of water over the skin combined with forced-air equipment (ventilator/fan) which creates a warm, dry microclimate around the skin and promotes water evaporation. 

One report found a cooling rate of 0.14°C/min by simply splashing copious amounts of water (20-40L) over the heat stroke patient and fanning continuously. 

The body cooling unit (BCU) developed by Khogali and Weiner was reported to be successful in treating heat stroke victims during the annual pilgrimage to Mecca, achieving a cooling rate

of 0.05°C/min.

2. Invasive Cooling Methods

Iced peritoneal lavage and gastric lavage are two invasive methods reported for body cooling. The rationale of invasive therapies is to bypass the body shell and achieve direct cooling of internal body organs.The use of iced peritoneal lavage and gastric lavage has yielded inconsistent results and is therefore not recommended. 

3. Pharmacologic Methods

Dantrolene impairs calcium release from the sarcoplasmic reticulum and by doing so reduces muscle excitation and contraction. It is used to treat malignant hyperthermia and neuroleptic malignant syndrome and is proposed to have a role in reducing core body temperature in exertional heat stroke.

However, studies have shown that there is no additional benefit in using dantrolene in the treatment of heat stroke.

Anti-pyretic, anti-inflammatory agents like paracetamol, nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids, as well as antibiotics have also been shown to have little or no

benefits in managing heat injury. Aspirin and paracetamol should be avoided because they may

trigger fulminant hepatitis in patients with heat stroke and heatinduced hepatic damage. 

Antibiotics are not routinely administered in heat stroke unless the patient develops an

infection or has suspected meningitis. The use of pharmacologic agents has not been shown to

accelerate body cooling in the treatment of heat stroke and is therefore not recommended.

4. Hydration And Hemodynamic Management

Although rapid and effective cooling is the cornerstone of treating heat stroke, the management of circulatory failure is also important Hypotension is associated with a mortality rate of 33% compared with 10% in patients without hypotension. While hydration should be administered, it is not without

complications.

Fluid resuscitation should be titrated to clinical endpoints of optimal heart rate, urine output and blood pressure. Patients who remain hypotensive after initial fluid and cooling therapy should

be considered for invasive hemodynamic monitoring.182 However, invasive hemodynamic monitoring should be avoided in patients with complications of DIVC. 

The initial management of heatstroke should include adequate fluid replacement to restore blood pressure and tissue perfusion. Intravenous fluid replacement should be carefully titrated to

clinical endpoints to avoid fluid overload and iatrogenic

pulmonary oedema.

5. Treatment of complications of heat stroke

                                  

Seizure

For heat stroke patients, short acting benzodiazepines are generally effective in controlling seizures.

Hypotension

In patients with hypotension that is refractive to intravenous therapy, vasopressors may be indicated, but should be used with caution because catecholamines can lead to increased heat

production. 

Rhabdomyolysis

Rhabdomyolysis is a serious complication of exertional heat stroke and the monitoring of urine output is crucial. Intravenous fluids and diuretics (e.g. mannitol at 0.25g/kg) help to maintain renal blood flow and may prevent renal destruction in heat stroke.Alkalinisation has been recommended for rhabdomyolysis and hemofiltration should be

considered for severe cases.

Disseminated intra-vascular coagulation

Disseminated intra-vascular coagulation is an indication of poor prognosis and should be managed with blood products for bleeding accordingly.

Hepatic injury

Hepatic injury can result in coagulopathy and hepatitis. Non Steroidal Anti-Inflammatory Drugs (NSAIDs) and Paracetamol should be avoided in the treatment of exertional heat stroke as these may precipitate hepatic damage.

Hypoglycemia should be detected and treated.

Arrhythmia

Hypotension and cell death can lead to myocardial damage and arrhythmia. Many of the arrhythmias will resolve with cooling. Cardiac Monitoring should be used in a patient with heat stroke.

Metabolic Disorder

Muscle necrosis may occur so rapidly that hyperkalemia, hypocalcemia, and hyperphosphatemia become significant enough to cause cardiac arrhythmias and require immediate therapy. In the presence of renal failure, hemodialysis may be necessary.

Pulmonary injury

Pulmonary edema is a common complication of heatstroke and may be due to a number of factors, including fluid overload from aggressive rehydration, renal failure, congestive heart failure, and ARDS. 

Renal injury

AKI may occur because of direct thermal injury of the kidney, myoglobinuria, hypotension, and/or shock (acute tubular necrosis). Early manifestations of AKI include oliguria, low-grade proteinuria, and granular casts.

AKI initially is treated with intravenous fluids, diuretics, and correction of associated acid-base and electrolyte abnormalities. In the setting of rhabdomyolysis, mannitol may be the diuretic of choice because it does not interfere with the acid-base status of the urine, and it may have antioxidant activity. Furosemide may cause tubular acidosis and, therefore, may promote myoglobin deposition within the renal tubules. Once renal failure has set in, hemodialysis is the most effective therapy.

Source : www.moh.gov.sg

             www.dtic.mil

             emedicine.medscape.com

             www.aafp.org