What is EHI?

The Joint Service Publication on Climatic Illness and Injury in the Armed Forces (JSP 539)10 uses the term ‘heat illness’ to describe those instances where an individual becomes incapacitated as a result of a rise in core body temperature (Tc). When this occurs during physical exertion, the individual may be said to have experienced EHI. EHI is a complex disorder in which thermal homeostasis is disrupted by physiological, environmental and hereditary factors, acting in the setting of exertional heat stress.11 It may occur as an isolated event or affect individuals recurrently. In practice, presentation of EHI occurs across a clinical spectrum from mild symptoms, such as muscular weakness, headache and disproportionate fatigue, through to collapse, coma and death.10

How is Tc maintained within a ‘safe’ range?

Excess body heat may arise endogenously such as from skeletal muscle contraction or exogenously (eg, solar radiation) and successful thermoregulation is dependent upon the individual's ability to dissipate this heat into the surrounding environment. The principal thermo-effector mechanisms are increased blood flow to the skin and superficial tissues and evaporation of sweat. The vasculature delivers heat from the core to the periphery so that it may be lost by conduction, convection and radiation (where ambient temperature allows) and by evaporation (where thermal sweating is effective). Failure of these mechanisms to achieve adequate heat dissipation results in thermal disequilibrium and rise in Tc. Unchecked, this process will critically influence the normal functioning of cells and tissues,12 with denaturation of proteins occurring at Tc greater than 44°C. In controlled laboratory settings, athletes tend to terminate exercise due to fatigue as Tc approaches 40°C13 and this has been taken to define the threshold for exertional hyperthermia.

How does Tc relate to risk of harm from EHI?

Circulatory compromise and tissue hypoxia have been observed during exertional hyperthermia14 but precise knowledge of how this state proceeds to EHI remains unknown. Various conceptual models exist to explain the observed biological phenomena (Figure 1). The development of exertional heat stroke (EHS) is the most severe manifestation of EHI in which a systemic inflammatory response arises in association with a syndrome of multiple organ dysfunction, predominated by encephalopathy.15 As the accepted definition of EHS incorporates a Tc threshold of 40°C, many research protocols adopt Tc >39.5°C as a key withdrawal criterion in volunteers subjected to exertional heat stress.

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Figure 1

Conceptual model of pathophysiology contributing to exertional heat illness and exertional heat stroke.

However, both exercise and thermal stress are known to induce common physiological responses and physical performance is affected by exertional hyperthermia in a complex manner that is not uniformly detrimental.16 In the British Army, studies to determine Tc responses to specific forms of arduous training have been commissioned by the Ministry of Defence in both officer cadets at the Royal Military Academy Sandhurst (RMAS)17 and Parachute Regiment recruits on the Pegasus Company pre-parachute selection course (‘P Coy’).18 In certain events, such as the Steeplechase component of the RMAS Sovereign's Banner competition, Tc was observed to rise above 40°C in five of 10 monitored competitors, none of whom succumbed to EHI. On P Coy, one recruit successfully completed the ‘10-miler’ loaded march despite hitting a peak Tc of 42°C, whereas other individuals with lower peak Tc were withdrawn due to suspected EHI. Historically, it is training events of shorter duration and greater physical intensity, such as Log Races, that are more strongly associated with EHI. The data from both RMAS and P Coy indicate that events of this nature generate lower peak Tc than longer endurance-type events, but may lead to a greater rate of metabolic heat storage. It could be hypothesised that rate of Tc rise, rather than absolute Tc attained, has a greater bearing on the evolution of EHI in certain vulnerable individuals.

These findings suggest that the validity of 39.5°C as an absolute Tc threshold for withdrawal of military volunteers from thermal studies might reasonably be questioned. Furthermore, the need for future research to define the importance of rate of Tc rise during exercise is also highlighted. Methods that more precisely predict, mitigate or manipulate Tc rise during exertional heat stress may play a future role in prevention of EHI. Research to improve understanding of the thermo-effector response should be considered in relation to this challenge.

Who is at risk of EHI?

Among the mammals, humans rank with the greatest capacity for exercising in extreme heat,19 yet EHI is among the leading causes of death in young athletes each year.20 EHI commonly affects individuals who sustain a high rate of work in hot weather,21 although the risk is not exclusive to hot climates and most UK military casualties are sustained in temperate zones.10 The majority of cases of EHS occur in endurance athletes and the military, these individuals being highly motivated and often unwilling or unable to curtail their own work rate.2,1 ,2,2 In the USA, American football is the leading cause of fatalities due to EHS in organised sport23 and investigations into Tc rise in experienced footballers have highlighted the interaction between metabolic heat production and dress state. Certain military uniforms, such as chemical biological radiological and nuclear (CBRN) protective clothing, prevent the dissipation of metabolic heat and also increase metabolic rate and internal heat production when worn during exercise.24––26 This combination of increased heat production and decreased heat loss was shown to increase rate of core temperature rise by 38% when torso-body armour and combat helmet were worn during simulated low-tempo urban patrolling conditions in a tropical environment.27 It is anticipated that future provision of mandatory personal protective equipment and the advent of fully integrated clothing/protection systems—which are important developments intended to reduce ballistic trauma in military populations—will be accompanied by concurrent enquiry into whether thermal burden and EHI risk are also affected.

How common is EHI?

The most recent annual reporting data on EHI in the British Army28 identified 74 cases from a serving population of 101 300 (0.73 per 1000 person-years).29 In the same year (2011), 10 Regular UK Army personnel were medically discharged due to EHI and no deaths were attributed to heat.30 Over the 10-year period, 2002–2012, four EHI-related deaths were recorded by the UK Defence Statistics organisation (previously known as the Defence Analytical Services Agency).30

However, calculated rates of EHI among military populations are subject to error and problems of interpretation that may arise both in the numerator data (ie, the number of EHI cases that are recorded) and from the selected denominator (ie, the total population that is perceived to be at risk of EHI). The former will vary according to recognition and reporting patterns, which are themselves subject to the capability and capacity of the healthcare environment in which EHI occurs and would be expected to under-estimate EHI as these functions become more limited (eg, moving ‘forwards’ in the deployed environment, from Role 3 towards Role 1). The denominator may conceal tremendous variation in risk of EHI (eg, individuals undertaking arduous training versus those with chronic physical injuries that prevent strenuous exertion), both between the sampled individuals and on an intra-individual basis, as activities and physical performance limit change across a reporting year.

By way of illustration, the United States Disease Defense Medical Surveillance System identified crude rates of heat stroke (0.25 per 1000 person-years) and ‘other heat injury’ (1.82 per 1000 person-years) for members of the United States Armed Forces during the year 2011.31 However, these data were based on records of medical encounters at fixed medical facilities; EHI cases incurred on training exercises and deployments and treated in the field, at sea or at deployed medical facilities were not captured. The requirement for the proper epidemiological collection, analysis and interpretation of data, including that from operational deployments, remains extant and is necessary for defining the true burden and nature of EHI in modern military populations.

How can EHI be predicted?

Risk factors for EHI are well described (Box 1). However, serious EHI can occur in personnel practising sound heat mitigation strategies and in those who are not judged to be at high risk. For example, over 50% of EHS cases among US Marine Corps recruits in-training were considered low or medium risk for EHI prior to becoming casualties.32 Furthermore, while attention to JSP 539 by Commanders is central to reducing EHI rates, the often urgent requirements placed on military personnel—especially in an operational context—may not always allow for absolute avoidance of all known risk factors. As EHI can occur for the first time in individuals who have been exposed to similar conditions on many previous occasions, without affecting other individuals exposed alongside them, there appears to be a degree of individual vulnerability that varies according to intrinsic host factors.33

Among individuals assessed as physiologically ‘heat intolerant’, significantly decreased expression of genetic transcription factors has been identified during exertional heat stress, suggesting failure of cellular adaptation.34 Other research has identified around 700 genes that may be activated or suppressed by exertional heat stress following an episode of EHS, suggesting that genome screening could inform individual predisposition to EHI or susceptibility to more severe forms.35 It is known that polymorphisms of the ACE gene confer increased thermal tolerance36 and the role of the related renin–angiotensin–aldosterone system in thermoregulation presents an intriguing avenue of scientific exploration.

The interaction between the immune system and exertional heat stress is another area of interest, where ongoing investigation may help to explain the idiosyncratic nature of EHI. It has been shown that a proportion of the rise in body temperature during exercise can be attributed to systemic inflammatory responses, including leucocytosis and cytokinaemia.37 Changes in the level of the cytokine interleukin-6 (IL-6) are also linked to thermal strain during exercise; IL-6 has received attention as a potential ‘biomarker’ for identifying individuals at increased risk of EHI.38 The putative role of intestinal barrier dysfunction in EHI,15 in which translocation of gut lipopolysaccharide may lead to a systemic inflammatory response syndrome, suggests possible parallels between EHI, sepsis and trauma. Mutual benefits may be achieved from research within and between these fields.