High environmental temperature, high humidity, strenuous exercise or impaired heat dissipation may cause a variety of heat disorders. They include heat syncope, heat oedema, heat cramps, heat exhaustion and heat stroke as systemic disorders, and skin lesions as local disorders.
Heat cramps, heat exhaustion and heat stroke are of clinical importance. The mechanisms underlying the development of these systemic disorders are circulatory insufficiency, water and electrolyte imbalance and/or hyperthermia (high body temperature). The most severe of all is heat stroke, which may lead to death unless promptly and properly treated.
Two distinct populations are at risk of developing heat disorders, excluding infants. The first and the larger population is the elderly, especially the poor and those with chronic conditions, such as diabetes mellitus, obesity, malnutrition, congestive heart failure, chronic alcoholism, dementia and the need to use medications that interfere with thermoregulation. The second population at risk of suffering heat disorders comprises healthy individuals who attempt prolonged physical exertion or are exposed to excessive heat stress. Factors predisposing active young people to heat disorders, other than congenital and acquired sweat gland dysfunction, include poor physical fitness, lack of acclimatization, low work efficiency and a reduced ratio of skin area to body mass.
Syncope is a transient loss of consciousness resulting from a reduction of cerebral blood flow, preceded frequently by pallor, blurring of vision, dizziness and nausea. It may occur in persons suffering from heat stress. The term heat collapse has been used synonymously with heat syncope. The symptoms have been attributed to cutaneous vasodilatation, postural pooling of blood with consequently diminished venous return to the heart, and reduced cardiac output. Mild dehydration, which develops in most persons exposed to heat, contributes to the probability of heat syncope. Individuals who suffer from cardiovascular diseases or who are unacclimatized are predisposed to heat collapse. The victims usually recover consciousness rapidly after they are laid supine.
Mild dependent oedema-that is, swelling of the hands and feet-may develop in unacclimatized individuals exposed to a hot environment. It typically occurs in women and resolves with acclimatization. It subsides in several hours after the patient has been laid in a cooler place.
Heat cramps may occur after heavy sweating brought about by prolonged physical work. Painful spasms develop in limb and abdominal muscles subjected to intensive work and fatigue, while body temperature hardly rises. These cramps are caused by the salt depletion that results when the loss of water due to prolonged heavy sweating is replenished with plain water containing no supplementary salt and when the sodium concentration in the blood has fallen below a critical level. Heat cramps themselves are a relatively innocuous condition. The attacks are usually seen in physically fit individuals who are capable of sustained physical exertion, and once were called “miner’s cramps” or “cane-cutter’s cramps” because they would often occur in such labourers.
The treatment of heat cramps consists of cessation of activity, rest in a cool place and replacement of fluid and electrolytes. Heat exposure should be avoided for at least 24 to 48 hours.
Heat exhaustion is the most common heat disorder encountered clinically. It results from severe dehydration after a huge amount of sweat has been lost. It occurs typically in otherwise healthy young individuals who undertake prolonged physical exertion (exertion-induced heat exhaustion), such as marathon runners, outdoor sports players, military recruits, coal miners and construction workers. The basic feature of this disorder is circulatory deficiency due to water and/or salt depletion. It may be considered an incipient stage of heat stroke, and if left untreated, it may eventually progress to heat stroke. It has been conventionally divided into two types: heat exhaustion by water depletion and that by salt depletion; but many cases are a mixture of both types.
Heat exhaustion by water depletion develops as a result of prolonged heavy sweating and insufficient water intake. Since sweat contains sodium ions in a concentration ranging from 30 to 100 milliequivalents per litre, which is lower than that in plasma, a great loss of sweat brings about hypohydration (reduction in body water content) and hypernatraemia (increased sodium concentration in plasma). Heat exhaustion is characterized by thirst, weakness, fatigue, dizziness, anxiety, oliguria (scanty urination), tachycardia (rapid heartbeat) and moderate hyperthermia ( or above). Dehydration also leads to a decline in sweating activity, a rise in skin temperature, and increases in plasma protein and plasma sodium levels and in the haematocrit value (the ratio of blood cell volume to blood volume).
Treatment consists of allowing the victim to rest in a recumbent posture with the knees raised, in a cool environment, wiping the body with a cool towel or sponge and replacing fluid loss by drinking or, if oral ingestion is impossible, by intravenous infusion. The amounts of water and salt replenishment, body temperature and body weight should be monitored carefully. Water ingestion should not be regulated according to the victim’s subjective feeling of thirst, especially when fluid loss is replenished with plain water, because dilution of the blood readily induces disappearance of thirst and dilution diuresis, thus delaying the recovery of body fluid balance. This phenomenon of insufficient water ingestion is called voluntary dehydration. Furthermore, a salt-free water supply may complicate heat disorders, as described below. Dehydration of over 3% of body weight should always be treated by water and electrolyte replacement.
Heat exhaustion by salt depletion results from prolonged heavy sweating and replacement of water and insufficient salt. Its occurrence is promoted by incomplete acclimatization, vomiting and diarrhoea, and so on. This type of heat exhaustion usually develops a few days after the development of water depletion. It is most commonly encountered in sedentary elderly individuals exposed to heat who have drunk a large amount of water in order to quench their thirst. Headache, dizziness, weakness, fatigue, nausea, vomiting, diarrhoea, anorexia, muscle spasms and mental confusion are common symptoms. In blood examinations, decrease in plasma volume, increases in the haematocrit and in plasma protein levels, and hypercalcaemia (excess blood calcium) are noted.
Early detection and prompt management are essential, the latter consisting of letting the patient rest in a recumbent posture in a cool room and providing for replacement of water and electrolytes. The osmolarity or specific gravity of the urine should be monitored, as should urea, sodium and chloride levels in the plasma, and body temperature, body weight, and water and salt intake should also be recorded. If the condition is adequately treated, victims generally feel well within a few hours and recover without sequelae. If not, it may readily proceed to heat stroke.
Heat stroke is a serious medical emergency which may result in death. It is a complex clinical condition in which uncontrollable hyperthermia causes tissue damage. Such an elevation of body temperature is caused initially by severe heat congestion due to excessive heat load, and the resultant hyperthermia induces dysfunction of the central nervous system, including failure of the normal thermoregulatory mechanism, thus accelerating elevation of the body temperature. Heat stroke occurs basically in two forms: classical heat stroke and exertion-induced heat stroke. The former develops in very young, elderly, obese or unfit individuals undertaking normal activities during prolonged exposure to high environmental temperatures, whereas the latter occurs particularly in young, active adults during physical exertion. In addition, there is a mixed form of heat stoke presenting features consistent with both of the above forms.
Elderly individuals, particularly those who have underlying chronic illness, such as cardiovascular diseases, diabetes mellitus and alcoholism, and those taking certain medications, especially psychotropic drugs, are at a high risk of classical heat stroke. During sustained heat waves, for example, the mortality rate for the population older than 60 years has been recorded as more than ten times greater than that for the population aged 60 and under. A similarly high mortality in the elderly population has also been reported among Muslims during the Mecca pilgrimage, where the mixed form of heat stroke has been found to be prevalent. Factors predisposing the elderly to heat stroke, other than chronic diseases as mentioned above, include reduced thermal perception, sluggish vasomotor and sudomotor (sweating reflex) responses to changes in thermal load, and reduced capacity for acclimatization to heat.
Individuals who work or exercise vigorously in hot, humid environments are at a high risk of exertion-induced heat illness, whether heat exhaustion or heat stroke. Athletes undergoing high physical stress can fall victim to hyperthermia by producing metabolic heat at a high rate, even when the environment is not very hot, and have often suffered heat stress illness as a result. Relatively unfit non-athletes are at a lesser risk in this regard as long as they realize their own capacity and limit their exertions accordingly. However, when they play sports for fun and are highly motivated and enthusiastic, they often try to exert themselves at an intensity beyond that for which they have been trained, and may succumb to heat illness (usually heat exhaustion). Poor acclimatization, inadequate hydration, unsuitable dress, alcohol consumption and skin illness causing anhidrosis (reduction in or lack of sweating), notably prickly heat (see below), all aggravate the symptoms.
Children are more susceptible to heat exhaustion or heat stroke than adults. They produce more metabolic heat per unit mass, and are less able to dissipate heat because of a relatively low capacity to produce sweat.
Clinical features of heat stroke
Heat stroke is defined by three criteria:
1. severe hyperthermia with a core (deep body) temperature usually exceeding
2. disturbances of the central nervous system
3. hot, dry skin with cessation of sweating.
The diagnosis of heat stroke is easy to establish when this triad of criteria is met. However, it may be missed when one of those criteria is absent, obscure or overlooked. For example, unless core temperature is measured properly and without delay, severe hyperthermia may not be recognized; or, in a very early stage of exertion-induced heat stroke, sweating may still persist or may even be profuse and the skin may be wet.
The onset of heat stroke is usually abrupt and without precursory symptoms, but some patients with impending heat stroke may have symptoms and signs of disturbances of the central nervous system. They include headache, nausea, dizziness, weakness, drowsiness, confusion, anxiety, disorientation, apathy, aggressiveness and irrational behaviour, tremor, twitching and convulsion. Once heat stroke occurs, disturbances of the central nervous system are present in all cases. The level of consciousness is often depressed, deep coma being most common. Seizures occur in the majority of cases, especially in physically fit individuals. Signs of cerebellar dysfunction are prominent and may persist. Pin-pointed pupils are frequently seen. Cerebellar ataxia (lack of muscular coordination), hemiplegia (paralysis of one side of the body), aphasia and emotional instability may persist in some of survivors.
Vomiting and diarrhoea often occur. Tachypnoea (rapid breathing) is usually present initially and the pulse may be weak and rapid. Hypotension, one of the most common complications, results from marked dehydration, extensive peripheral vasodilatation and eventual depression of cardiac muscle. Acute renal failure may be seen in severe cases, especially in exertion-induced heat stroke.
Haemorrhages occur in all parenchymal organs, in the skin (where they are called petechiae) and in the gastro-intestinal tract in severe cases. Clinical haemorrhagic manifestations include melaena (dark-coloured, tarry faeces), haematemesis (blood vomiting), haematuria (bloody urine), haemoptysis (spitting blood), epistaxis (nosebleed), purpura (purple spots), ecchymosis (black and blue marks) and conjunctival haemorrhage. Intravascular coagulation occurs commonly. Haemorrhagic diathesis (bleeding tendency) is usually associated with disseminated intra-vascular coagulation (DIC). DIC occurs predominantly in exertion-induced heat stroke, where the fibrinolytic (clot-dissolving) activity of plasma is increased. On the other hand, a decrease in platelet count, prolongation of prothrombin time, depletion of coagulation factors and increased level of fibrin degradation products (FDP) are provoked by whole-body hyperthermia. Patients with evidence of DIC and bleeding have higher core temperature, lower blood pressure, lower arterial blood pH and , a higher incidence of oliguria or anuria and of shock, and a higher mortality rate.
Shock is also a common complication. It is attributable to peripheral circulatory failure and is aggravated by DIC, which causes dissemination of clots in the microcirculatory system.
Treatment of heat stroke
Heat stroke is a medical emergency that requires prompt diagnosis and rapid and aggressive treatment to save the patient’s life. Proper measurement of core temperature is mandatory: rectal or oesophageal temperature should be measured by using a thermo-meter which can read up to . Measurement of oral and axillary temperatures should be avoided because they can vary significantly from real core temperature.
The objective of treatment measures is to lower body temperature by reducing heat load and promoting heat dissipation from the skin. The treatment includes moving the patient to a safe, cool, shady and well-ventilated place, removing unnecessary clothing, and fanning. Cooling the face and head may promote beneficial brain cooling.
The efficiency of some cooling techniques has been questioned. It has been argued that placing cold packs over major blood vessels in the neck, groin and axillae and immersion of the body in cold water or covering it with iced towels may promote shivering and cutaneous vasoconstriction, thus actually impeding cooling efficiency. Traditionally, immersion in an ice-water bath, combined with vigorous skin massage to minimize cutaneous vasoconstriction, has been recommended as the treatment of choice, once the patient is brought to a medical facility. This method of cooling has several disadvantages: there are the nursing difficulties posed by the need to administer oxygen and fluids and to monitor blood pressure and the electrocardiogram continuously, and there are the hygienic problems of contamination of the bath with the vomitus and diarrhoea of comatose patients. An alternative approach is to spray a cool mist over the patient’s body while fanning to promote evaporation from the skin. This method of cooling can reduce the core temperature by 0.03 to .
Measures to prevent convulsions, seizures and shivering should also be initiated at once. Continuous cardiac monitoring and determination of serum electrolyte levels and arterial and venous blood-gas analysis are essential, and intravenous infusion of electrolyte solutions at a relatively low temperature of approximately , together with controlled oxygen therapy, should be commenced in a timely fashion. Tracheal intubation to protect the airway, insertion of a cardiac catheter to estimate central venous pressure, placement of a gastric tube and insertion of a urinary catheter may also be included among additional recommended measures.
Prevention of heat stroke
For the prevention of heat stroke, a wide variety of human factors should be taken into account, such as acclimatization, age, build, general health, water and salt intake, clothing, peculiarities of religious devotion and ignorance of, or liability to neglect, regulations intended to promote public health.
Prior to physical exertion in a hot environment, workers, athletes or pilgrims should be informed of the work load and the level of heat stress they may encounter, and of the risks of heat stroke. A period of acclimatization is recommended before vigorous physical activity and/or severe exposure is risked. The level of activity should be matched to the ambient temperature, and physical exertion should be avoided or at least minimized during the hottest hours of the day. During physical exertion, free access to water is mandatory. Since electrolytes are lost in sweat and the opportunity for voluntary ingestion of water may be limited, thus delaying restitution from thermal dehydration, electrolytes should also be replaced in case of profuse sweating. Proper clothing is also an important measure. Clothes made of fabrics which are both water-absorbent and permeable to air and water vapour facilitate heat dissipation.
Miliaria is the most common skin disorder associated with heat load. It occurs when the delivery of sweat onto the skin surface is prevented due to obstruction of the sweat ducts. Sweat retention syndrome ensues when anhidrosis (inability to release sweat) is widespread over the body surface and predisposes the patient to heat stroke.
Miliaria is commonly induced by physical exertion in a hot, humid environment; by febrile diseases; by the application of wet compresses, bandages, plaster casts or adhesive plaster; and by wearing poorly permeable clothes. Miliaria can be classified into three types, according to the depth of sweat retention: miliaria crystallina, miliaria rubra and miliaria profunda.
Miliaria crystallina is caused by retention of sweat within or just beneath the horny layer of the skin, where tiny, clear, non-inflammatory blisters can be seen. They typically appear in “crops” after severe sunburn or during a febrile illness. This type of miliaria is otherwise symptomless, the least distressing, and heals spontaneously in a few days, when the blisters break out to leave scales.
Miliaria rubra occurs when intense heat load causes prolonged and profuse sweating. It is the most common type of miliaria, in which sweat accumulates in the epidermis. Red papules, vesicles or pustules are formed, accompanied by burning and itching sensations (prickly heat). The sweat duct is plugged at the terminal portion. The production of the plug is attributable to the action of resident aerobic bacteria, notably cocci, which increase in population greatly in the horny layer when it is hydrated with sweat. They secrete a toxin which injures the horny epithelial cells of the sweat duct and provokes an inflammatory reaction, precipitating a cast within the lumen of the sweat duct. Infiltration by leukocytes creates an impaction which completely obstructs the passage of sweat for several weeks.
In miliaria profunda, sweat is retained in the dermis, and produces flat, inflammatory papules, nodules and abscesses, with less itching than in miliaria rubra. The occurrence of this type of miliaria is commonly confined to the tropics. It may develop in a progressive sequence from miliaria rubra after repeated bouts of profuse sweating, as the inflammatory reaction extends downwards from the upper skin layers.
Tropical anhidrotic asthenia. The term achieved currency during the Second World War, when troops deployed to tropical theatres suffered from heat rash and heat intolerance. It is a modality of sweat retention syndrome encountered in hot, humid tropical environments. It is characterized by anhidrosis and miliaria-like rashes, accompanied by symptoms of heat congestion, such as palpitation, rapid pulsation, hyperthermia, headache, weakness and gradually to rapidly progressing inability to tolerate physical activity in the heat. It is usually preceded by widespread miliaria rubra.
Treatment. The initial and essential treatment of miliaria and sweat retention syndrome is to transfer the affected person to a cool environment. Cool showers and gentle drying of the skin and the application of calamine lotion may attenuate the patient’s distress. Application of chemical bacteriostats is effective in preventing the expansion of microflora, and is preferable to the use of antibiotics, which may lead these micro-organisms to acquire resistance.
The impactions in the sweat duct slough off after about 3 weeks as a result of epidermal renewal.