heat-related illness and death


The pathological investigation of deaths thought to be due to heat-stroke, or hyperthermia can be challenging. This article, guest authored by Dr Andrew Davison (Senior Lecturer in Forensic Pathology at the Wales Institute of Forensic Medicine), explores the pathophysiology of heat-related deaths.


Heat-illness & heat-related deaths in the media



The process of thermoregulation ensures that at rest and in comfortable environmental conditions the human body’s core temperature is closely maintained at 37 degrees Celcius.

Under exercise/heat stress "normal” body temperature will be higher. Temperature receptors in the skin and organs transmit information to the brain – particularly the hypothalamus – which co-ordinates a response to hyperthermia e.g. reduced blood flow to some organs (liver, gut) and increased blood flow to the skin to facilitate heat loss (Hashim 2010 and Epstein and Roberts 2011).

Heat is generated within the body by metabolic processes and is absorbed from the environment when ambient temperature is higher than skin temperature (Epstein and Roberts 2011).

Heat loss occurs at two levels:

  • intrinsic, from the core to the skin or respiratory tract;
  • extrinsic, from the skin to the environment.

The extrinsic pathway occurs from four environmentally-mediated heat transferring mechanisms:

  • conduction (heat transfer between two directly apposed objects with the direction of heat flow from higher to lower temperature),
  • convection (the movement of moleculesin a gas or liquid which facilitates conduction), 
  • radiation (via electromagnetic rays where the ambient temperature is below core body temperature), and 
  • evaporation (change from liquid to gas or vapour form, principally sweating). Heat loss from evaporation is limited at high humidity (Nixdorf-Miller et al 2006).

Heat-related illness can occur when high ambient temperature exceeds the ability of the body to dissipate heat.

Strenuous exercise in hot humid conditions is an example of increased heat production combined with impaired heat dissipation (Hashim 2010 and Epstein and Roberts 2011).

Heat-related illness is a continuum; the mildest form is heat intolerance, followed by heat stress, heat exhaustion and the most severe form - heatstroke (Hashim 2010).

Heatstroke is a life-threatening disorder due to complete loss of thermoregulation. It is characterised by a core body temperature above 40 degrees C and dysfunction of multiple organs/systems e.g. brain, kidneys, liver, muscle, cardiovascular, gastrointestinal. Clinically there may be biochemical evidence of metabolic acidosis, respiratory alkalosis, hepatic (liver) injury and abnormal coagulation (Hashim 2010, Epstein and Roberts 2011, and Leon and Helwig 2010).

Central nervous system dysfunction may manifest as mental state changes, including confusion, delerium, combativeness, seizures or coma at the time of collapse (Leon and Helwig 2010).

Heatstroke is classified as passive or exertional. Young fit individuals may experience exertional heatstroke while performing strenuous physical activity in temperate or hot climates. Military personnel are at increased risk of heat-related illness (Hashim 2010 and Leon and Helwig 2010).

Exertional heatstroke is a function of both intrinsic and extrinsic modulators.

  • Intrinsic modulators e.g. genetics, fitness, acclimatisation, illness, medications and sleep quality can alter individual risk and outcomes. 
  • Extrinsic modulators e.g. exercise intensity and duration, clothing and equipment, ambient temperature, relative humidity and solar radiation can affect group risk and outcomes (Epstein and Roberts 2011).

Multi-organ failure is the ultimate mode of death, and heat-related mortality is high – ranging between 33 and 80%.

Terminal events include shock, arrhythmias,myocardial infarction, renal failure, liver failure and various neurological dysfunctions (Hashim 2010, Leon and Helwig 2010, and Sucholeiki 2005).

The development of heatstroke and progression to multi-organ dysfunction is a complex interplay of several factors:

  • acute physiological alterations associatedwith hyperthermia e.g. circulatory failure, hypoxia, increased cellularmetabolic demands;
  • direct cellular damage due to heat;
  • the systemic inflammatory response; and
  • failure of the coagulation system (Epstein and Roberts 2011, and Yan et al 2006).

Drugs - both prescribed and illicit - may induce hyperthermia or lower the threshold for heatstroke.

  • Prescribed substances include anti-epileptic medications, anti-cholinergics, psychotropics, antihistamines, diuretics and tricyclic anti-depressants. 
  • Illicit substances include ecstasy, amphetamine, cocaine and ephedrine.

Some of the substances work by affecting the concentrations of neurotransmitters in the hypothalamus and others interfere with vascular constriction/ dilation, which may affect the ability to lose heat through sweating (Hashim 2010 and Sucholeiki 2005).

Other risk factors that can lower the threshold for heatstroke include: dehydration, fatigue, poor physical conditioning, non-acclimatisation, insufficient water, high heat and humidity (Sucholeiki 2005).

Why some cases progress to heatstroke and others do not is unclear but it appears that genetic differences (polymorphisms) may determine susceptibility i.e. it is likely there is an individual variability to tolerating temperature changes (Epstein and Roberts 2011, Sucholeiki 2005, and Yeo 2004).

It has been stated that many cases of exertional heatstroke are preventable. Strategies include drinking water or non-alcoholic fluids frequently and reducing strenuous activities during the hottest times of the day (Yeo 2004).

Lack of heat acclimatisation is frequently associated with exercise and work-related hyperthermia in hot conditions. Acclimatisation – the incremental tolerance to a warmer environment – requires one to two weeks. Unacclimatised individuals undergoing strenuous activity generate and retain heat, which may result in severe heatillness or death. Physical training also improves tolerance of heat during exertion compared with those who are not conditioned (Nixdorf-Miller et al 2006, Sucholeiki 2005, and Yeo 2004).

Rapid reduction of body temperature is associated with improved survival and most patients who receive prompt and aggressive treatment recover from heatstroke.

The greatest number of deaths occur when treatment is delayed for over two hours. The key to successful resuscitation of heatstroke victims is early recognition and rapid cooling (Epstein and Roberts 2011, Sucholeiki 2005, and Yeo 2004).

post mortem findings


The post-mortem diagnosis of heat-related deaths presents certain difficulties.

Firstly, pre-terminal or terminal body temperatures are often not available. Additionally, naked-eye and microscopic findings are non-specific or inconclusive and depend on the duration of survival after exposure.

The diagnosis of hyperthermia is based on scene investigation, the circumstances of death, and the reasonable exclusion of other causes of death.

A heat-related cause of death may be assumed if the investigations provide compelling evidence of continuous exposure to a hot environment, and fail to identify an independent cause of death (Nixdorf-Miller et al 2006, and Palmiere and Mangin 2013).

The non-specific post-mortem findings in cases of fatal heatstroke include: pulmonary and cerebral oedema, necrosis of the liver, neuronal degeneration of the brain, rhabdomyolysis (breakdown of muscle), tubular casts in the kidneys and signs of disseminated intravascular coagulation e.g. fibrin thrombi in small blood vessels (Palmiere and Mangin 2013).

The post-mortem biochemistry findings are related to dehydration, electrolyte disturbance and skeletal muscle damage. They include increased serum creatinine, mild-to-moderate elevation of urea, and myoglobinuria, however, the diagnosis of heat-related fatalities cannot be based on post-mortem biochemical analyses alone (Palmiere and Mangin 2013).

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