Introduction

Heat-related disorders have a broad range of potential aetiologies and manifestations. In some the primary disorder is a failure of thermal homoeostasis, whereas in others the hyperthermia is secondary to other processes. The major heat-related illnesses to consider are heat exhaustion and exercise-associated collapse (EAC), heatstroke, neuroleptic malignant syndrome, serotonin toxicity and malignant hyperthermia. Although of different aetiologies they share much common ground, particularly with regard to complications and treatment.

Epidemiology and pathophysiology

Heat exhaustion and EAC are the most common heat-related illnesses presenting to emergency departments (EDs). Heat exhaustion occurs where substantial losses of fluid and electrolytes as sweat are inadequately replaced, and is most commonly observed in athletes and manual workers. The primary pathophysiological mechanisms are dehydration and intravascular volume depletion, but may include electrolyte loss and exercise-induced respiratory alkalosis. EAC manifests at the end of a race when muscle pump enhanced venous return ceases and cardiac output drops. This leads to collapse, often with a brief loss of consciousness.

The other, more serious, heat-related disorders are all associated with hyperthermia, which if not treated promptly results in similar pathophysiology at a cellular and organ system level. A core body temperature greater than 41°C results in progressive denaturing of a number of vital cellular proteins, failure of vital energy-producing processes and loss of cell membrane function. At a cellular level the exact mechanisms leading to loss of cell membrane function and cell death in heat illness remain uncertain. At an organ system level these changes may manifest as rhabdomyolysis, acute pulmonary oedema, disseminated intravascular coagulation, cardiovascular dysfunction, electrolyte disturbance, renal failure, liver failure and permanent neurological damage.¹ Any or all of these complications must be expected in severe heat illness.

Heatstroke shares some aetiological similarities with heat exhaustion but the hallmark of heatstroke is failure of the hypothalamic thermostat, leading to hyperthermia and the associated additional pathophysiological features described above. Clinically, heatstroke can be divided into ‘exertional heatstroke’ due to exercise in a thermally stressful environment, and ‘classic heatstroke’, which occurs in patients with impaired thermostatic mechanisms. Common risk factors for heatstroke are listed in Table 28.1.1.

Table 28.1.1 Heatstroke risk factors

Certain drugs produce hyperthermia by mechanisms in addition to interference with thermostatic function. In severe serotonin toxicity and neuroleptic malignant syndrome, increased motor activity and central resetting of the hypothalamic thermostat combine to produce hyperthermia. In the case of serotonin toxicity these effects are a consequence of a relative excess of central nervous system serotonin, whereas in neuroleptic malignant syndrome dopamine depletion or dopamine receptor blockade is responsible.

The elevation of central nervous system serotonin in serotonin toxicity is usually associated with combinations of serotoninergically active drugs, taken either therapeutically or in overdose. The incidence of serotonin toxicity when such combinations are taken is not known, but is low, and there is much individual variation in susceptibility.² The syndrome is rarely precipitated by a single serotoninergic agent. Drugs associated with the serotonin syndrome are listed in Table 28.1.2. The most commonly implicated combinations are MAOI with SSRI, MAOI with tricyclics, and MAOI with pethidine.

Table 28.1.2 Drugs causing severe serotonin toxicity

Neuroleptic malignant syndrome (NMS) is a rare idiosyncratic reaction to neuroleptic agents with an incidence of between 0.02% and 3.0%, depending on the diagnostic criteria used. It occurs in response to a single agent, usually at therapeutic dosage. In individuals, the occurrence may be dose-related. Certain at-risk groups have been identified and are listed in Table 28.1.3.

Table 28.1.3 Risk factors for neuroleptic malignant syndrome

Malignant hyperthermia is a genetically inherited disorder in which triggering agents cause a release of sarcoplasmic Ca²⁺ stores. The resulting elevation of myoplasmic Ca²⁺ stimulates many intercellular processes, including glycolysis, muscle contraction and an uncoupling of oxidative phosphorylation. This leads to hyperthermia that, in contrast to neuroleptic malignant and serotonin syndromes, is purely peripheral in origin.

Prevention

Prevention of exertional heatstroke should focus on the education of at-risk groups. Dehydration limits the body’s cooling ability, so the value of maintaining adequate but not excessive fluid intake during extreme exertion should be stressed. As high ambient temperatures and high humidity predispose to exertional heatstroke, exertion in these environments should be limited.

Clinical features

Clinical investigation

Diagnosis of the hyperthermic disorders is based on the history, clinical picture and exclusion of alternative diagnoses. Investigations are thus directed towards excluding other possible causes of temperature elevation (e.g. infection, metabolic disorders) and evaluation of the specific complications of hyperthermia.

Patients with a presumed clinical diagnosis of heat exhaustion or EAC should still have serum electrolytes and creatine kinase measured, together with a dipstick urinalysis. Measurement of serum electrolytes will detect dilutional hyponatraemia and other electrolyte disorders. In heat exhaustion there should be no myoglobin in the urine and, at most, only minor elevation of serum muscle enzymes.

All other heat disorders warrant a far more extensive laboratory and radiological work-up, as multiorgan system dysfunction is the rule.⁶ Tests should include an ECG (electrocardiograph), serum electrolytes, arterial blood gases, disseminated intravascular coagulation (DIC) screen, liver function tests, muscle enzyme assays, renal function and urinalysis, serum glucose and a chest X-ray.

Treatment

Prognosis and disposition

In heatstroke both the maximum core temperature and the duration of temperature elevation are predictors of outcome. Prolonged coma and oliguric renal failure are poor prognostic signs.¹ Mortality is still of the order of 10%, but most survivors will not suffer long-term sequelae.¹ Any patient with suspected heatstroke should routinely be referred to the intensive care unit for ongoing care. Most cases of heat exhaustion and EAC will be suitable for short-stay ED treatment.

Prognosis in the drug-related group of hyperthermia is dependent largely on the degree to which the complications have progressed before definitive and aggressive treatment is begun. Again, early referral to intensive care is indicated. Even with appropriate treatment, mortality for malignant hyperthermia approaches 7%. After recovery, the patient’s medication regimen will need to be reassessed, although in the case of neuroleptic malignant syndrome it may be possible to slowly reintroduce a neuroleptic agent at a lower dose. With malignant hyperthermia future anaesthesia will need to be modified to avoid precipitating agents. In addition, family members should be tested for susceptibility.

Introduction

Hypothermia is defined as a core temperature of less than 35°C. This can be measured at a number of sites (including oesophageal, right heart, tympanic and bladder). Rectal remains the routine in most emergency departments (EDs), despite concerns at how rapidly it equilibrates to and reflects true core temperature. Conventionally, hypothermia is divided into three groups: mild (32–35°C), moderate (29–32°C) and severe (<29°C) on the basis of measured core temperature. In a field setting, where core temperature measurements may not be possible, moderate and severe are often grouped together as they typically share the clinical features of absence of shivering and altered mental state. These categorization systems can be used both out of and in hospital as a guide to selecting rewarming therapies and prognosis. Mild hypothermia is considered the stage where thermogenesis is still possible; moderate is characterized by a progressive failure of thermogenesis; and severe by adoption of the temperature of the surrounding environment (poikilothermia) and an increasing risk of malignant cardiac arrhythmia. Nevertheless, there are substantial differences between individuals in their response to hypothermia.

Epidemiology and pathophysiology

Hypothermia may occur in any setting or season.¹ True environmental hypothermia occurring in a healthy patient in an adverse physical environment is less common in clinical practice than that secondary to an underlying disorder. Common precipitants include injury, systemic illness, drug overdose and immersion, and are outlined in more detail in Table 28.2.1. The elderly are at greater risk of hypothermia because of reduced metabolic heat production and impaired responses to a cold environment.² Alcohol is a common aetiological factor and probably acts by a number of mechanisms, including cutaneous vasodilatation, altered behavioural responses, impaired shivering and hypothalamic dysfunction. Hypothermia in the ED setting is often associated with underlying infection.³

Table 28.2.1 Hypothermia aetiologies

Clinical features

Despite substantial individual variations it is still possible to describe the typical patient in each category of hypothermia. The clinical manifestations of hypothermia also depend on the underlying aetiology and any associated features. To guide management in a field setting, where rectal temperature measurements are impractical or dangerous, moderate and severe hypothermia are often grouped together.⁴

Mild hypothermia manifests clinically as shivering, apathy, ataxia, dysarthria and tachycardia. Moderate hypothermia is typically marked by a loss of shivering, altered mental state, muscular rigidity, bradycardia and hypotension. In severe hypothermia signs of life may become almost undetectable, with coma, fixed and dilated pupils, areflexia and profound bradycardia and hypotension. The typical cardiac rhythm of severe hypothermia is slow atrial fibrillation. This may degenerate spontaneously, or with rough handling, into ventricular fibrillation or asystole.

Many complications may also manifest as part of a hypothermia presentation, although at times it may be difficult to separate cause from effect. These include cardiac arrhythmias, thromboembolism, rhabdomyolysis, renal failure, disseminated intravascular coagulation and pancreatitis.

Clinical investigation

Mild hypothermia with shivering and without apparent underlying illness needs no investigation in the ED.

Moderate or severe hypothermia mandates a comprehensive work-up to seek common precipitants and complications that may not be clinically apparent.

Biochemical and haematological abnormalities are frequently associated with hypothermia,¹ although there is no consistent pattern. Blood tests that are indicated include sodium, potassium, glucose, renal function, calcium, phosphate, magnesium, amylase, creatine kinase, ethanol, full blood count, clotting profile and arterial blood gases. Blood gas results should be accepted at face value, rather than adjusting for the patient’s temperature.⁵

Impaired ciliary function, stasis of respiratory secretions or aspiration may be expected in moderate-to-severe hypothermia, so chest radiography should be routine. Other radiology may be indicated if a trauma-related aetiology is suspected.

A 12-lead electrocardiograph (ECG) and continuous ECG monitoring should be routine in moderate-to-severe hypothermia. The typical appearance is slow atrial fibrillation, with J or Osborn waves most prominent in leads II and V₃–V₆ (Fig. 28.2.1). The J wave is the extra positive deflection after the normal S wave, and is more obvious and more commonly seen with increasing severity of hypothermia.

Fig. 28.2.1 ECG in hypothermia: slow atrial fibrillation and J waves in leads II, V₃–V₆ in a patient with a core temperature of 23.9°C.

Treatment

Rewarming therapies

Rewarming therapies in hypothermia have generated substantial debate. Unfortunately, there are only limited clinical trials on which to base recommendations. Although more invasive and rapid techniques are advocated for more severe hypothermia, there is little evidence to support this advice. The traditional concern of afterdrop (a paradoxical initial drop in core temperature with rewarming) is probably of little or no relevance in a clinical setting.⁶

Rewarming therapies are broadly divided into three groups: endogenous rewarming, which allows the body to rewarm by its own endogenous heat production; external exogenous rewarming, which supplies heat to the outside of the body; and core exogenous rewarming, which applies the heat centrally. The classification of the common rewarming therapies is outlined in Table 28.2.2.

Table 28.2.2 Rewarming therapy classification

Endogenous rewarming	Warm, dry, wind-free environment
	Warmed intravenous fluids
External exogenous rewarming	Hot bath immersion
	Forced-air blankets
	Heat packs
	Body-to-body contact
Core exogenous rewarming	Warmed, humidified inhalation
	Body cavity lavage
	-peritoneal
	-pleural
	Extracorporeal

Endogenous rewarming is a mandatory component of any ED rewarming protocol. It consists of drying the patient, covering them with blankets, placing them in a warm and wind-free environment, and warming any intravenous or oral fluids that are administered. Endogenous rewarming alone can be expected to rewarm at a rate of about 0.75°C/h. For most patients above 32°C (the level at which shivering thermogenesis is typically preserved), endogenous rewarming is the only therapy required. The exception is the exhausted patient in whom shivering has ceased at a core temperature higher than expected. Although more sophisticated techniques, such as bath immersion, will more rapidly rewarm a mildly hypothermic patient, there is no evidence that an increased rewarming rate improves prognosis in this group.

In moderate hypothermia, endogenous heat production is likely to progressively fail and more aggressive exogenous rewarming therapies are indicated. Hot-bath immersion has the theoretical disadvantage of causing peripheral vasodilatation, with shunting of cool blood to the core and convective heat loss. This might be expected to increase core afterdrop and produce circulatory collapse. In fact, rewarming rates of at least 2.5°C/h with minimal afterdrop have been achieved using baths at 43°C.⁷ Nevertheless, substantial practical difficulties are obvious with monitoring a more seriously ill patient immersed in a bath. This method of rewarming can only be recommended for otherwise healthy patients who are expected to make a rapid recovery from accidental environmental hypothermia (e.g. immersion in very cold water).

The two therapies that have been best studied and are widely used in moderate hypothermia are forced-air rewarming and warm humidified inhalation.⁸ Forced-air rewarming is achieved by covering the patient with a blanket filled with air at 43°C. These devices direct a continuous current of air over the patient’s skin through a series of slits in the patient surface of the blanket. This method produces minimal, if any, afterdrop, is apparently without complication and, combined with warm humidified inhalation, should produce rewarming at about 2.5°C/h. The value of warm humidified inhalation is probably by preventing ongoing respiratory heat loss. Given its widespread availability and lack of complications, it seems reasonable to combine it with forced-air rewarming in moderate hypothermia.⁹ Body-to-body contact and chemical heat packs are often recommended as field treatments for all degrees of hypothermia. In mild hypothermia it seems that the benefit of any heat they deliver is negated by an inhibition of shivering thermogenesis. In more severe cases, where shivering is absent, it may be that even the small amount of exogenous heat they deliver is beneficial, but this remains unproven.

In severe hypothermia more aggressive exogenous rewarming therapies may be indicated in order to rapidly achieve core temperature above 30°C, the threshold below which malignant cardiac arrhythmias may occur spontaneously. When available, full cardiopulmonary bypass achieves rewarming rates of about 7.5°C/h without core afterdrop. Pleural lavage using large volumes of fluid warmed to 40–45°C through an intercostal catheter may be nearly as effective. Both techniques are clearly invasive and carry associated risks. These risks are certainly acceptable in a hypothermic arrest, but in the non-arrested patient a slower rate of rewarming using forced-air and warm humidified inhalation may be more appropriate.

A suggested rewarming algorithm based on the evidence available to date is reproduced in Fig. 28.2.2.

Fig. 28.2.2 A recommended rewarming algorithm in hypothermia.

Prognosis and disposition

Attempts at developing a valid outcome prediction model for hypothermia are likely to be frustrated by its multifactorial aetiology. Recovery with appropriate treatment is likely from accidental environmental hypothermia when there is no associated trauma. To date, the coldest patient to survive accidental hypothermia neurologically intact had an initial measured temperature of 13.7°C.¹⁰ Although increasing severity of hypothermia does worsen prognosis, the major determinant of outcome is the precipitating illness or injury. Reported mortality rates vary from 0 to 85%.

Mild hypothermics without associated illness or injury can be safely managed at home in the care of a responsible adult. Moderate hypothermia may be treatable in a short-stay observation ward, but often requires a longer inpatient stay to manage underlying illness or injury. Severe hypothermics are at risk of multiorgan system complications and should be considered for admission to an intensive care unit.

Introduction

This chapter focuses on medical problems that develop secondary to breathing gases at higher than normal atmospheric pressure (dysbarism). This usually occurs in the context of scuba (self-contained underwater breathing apparatus) diving, a popular recreational activity in Australasia. Diving is generally very safe, and serious decompression incidents occur approximately 1: 10 000 dives. However, because of a high participation rate, between 300 and 400 cases of decompression illness are treated in Australia each year.¹ It is estimated that 10 times that number of divers experience less serious health problems after diving. Emergency physicians are often the first medical staff to assess the diver after a diving accident and it is essential they understanding the risks and potential injuries.

Diving physics and physiology

An understanding of pressure and some gas laws is essential to understand the pathophysiology of diving injuries. Absolute pressure at sea level is 1 atmosphere (ATA). Multiple units are used to measure pressure (Table 28.3.1). For every 10 m a diver descends in sea-water, the pressure increases by 1 ATA. This pressure change impacts on gas spaces within the body according to Boyle’s Law.

Table 28.3.1 Atmospheric pressure at sea level in various units

Boyle’s Law states that at a constant temperature the volume of a gas varies inversely to the pressure acting on it:

where P = pressure, V = volume and k = constant.

The proportionate change in volume is greatest near the surface (Table 28.3.2).

Table 28.3.2 Depth vs pressure and gas volume (Boyle’s law)

Dalton’s law states that the total pressure (P_t) exerted by a mixture of gases is equal to the sum of the pressures of the constituent gases (P_x, P_y, P_z):

Therefore, as divers breathe air at increasing atmospheric pressure, the partial pressures of nitrogen and oxygen increase:

A diver breathing air at 40 m is inhaling a gas with a partial pressure of oxygen equivalent to breathing 100% oxygen at the surface. At partial pressures above 3 ATA, the PN₂ affects coordination and judgement (‘nitrogen narcosis’). Oxygen may also become toxic at partial pressures greater than 1 ATA. Recreational scuba diving generally has a limit of 40 m because of these effects.

Henry’s law states that at a constant temperature the amount of a gas that will dissolve in a liquid is proportional to the partial pressure of the gas in contact with the liquid:

where Q = volume of gas dissolved in a liquid, k = constant and P_gas = partial pressure of the gas.

Henry’s law is relevant in diving illness in that it is the basis of decompression illness (DCI). As the ambient pressure increases, the diver is exposed to increasing partial pressures of nitrogen, which dissolves in bodily fluids. The amount of nitrogen absorbed depends on both the depth (which determines the partial pressure of nitrogen) and the duration of the dive. Tissues also take up nitrogen at different rates depending on their blood supply and permeability. Eventually, the tissues become saturated with nitrogen and no further absorption occurs. As the diver ascends and ambient pressure decreases, the partial pressure of nitrogen in some tissues will exceed ambient pressure, resulting in tissue supersaturation. If the diver ascends slowly enough, nitrogen diffuses out of the tissues and is transported, safely dissolved in the blood, to the lungs for elimination. This is known as ‘off-gassing’.

If the diver ascends too rapidly, sufficient nitrogen bubbles will form in their body to cause decompression illness. Oxygen does not cause problems because it is rapidly metabolized by the tissues.