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This article describes the spectrum of exertional heat stroke (EHS) disorders requiring emergency admission to a Dublin hospital in participants of the 2014 Dublin City Marathon.
Specifically, the cases of three marathoners presenting with hyperthermia, altered neurological status and acute kidney injury (AKI), ranging from sub-clinical elevation in serum creatinine to severe rhabdomyolysis requiring renal replacement therapy, are discussed.
EHS represents one of several heat-related illnesses, which also include classic or non-exertional heat stroke, heat cramp, heat exhaustion, heat syncope and exertional hyponatraemia.
EHS classically affects young healthy individuals, such as competitive athletes, military personnel or labourers who engage in prolonged, strenuous activity. Dysregulation of the normal thermoregulatory systems leads to variable clinical consequences including biochemical abnormalities, cardiac arrhythmias, rhabdomyolysis, AKI and liver injury, seizures, coma and death.
EHS is a leading cause of morbidity and mortality in young athletes, with a peak incidence in the summer months and an under-recognition of its importance by many endurance athletes.
The diagnosis is based on the clinical presentation.
The diagnostic criteria are core body hyperthermia (>40°C) and symptoms or signs of end-organ damage, often initially central nervous system (CNS) dysfunction. Heatstroke is a potentially life-threatening condition, requiring prompt recognition and early implementation of cooling and other supportive measures to reduce the potential for adverse outcomes.
Unlike non-exertional heat stroke, EHS patients retain their ability to sweat and hence the core temperature may have fallen when they present for medical attention, requiring a heightened index of suspicion. Investigations may reveal features of rhabdomyolysis, AKI, hepatitis and coagulopathy, similar to that seen in disseminated intravascular coagulopathy. Heat stroke is a medical emergency with a high potential for mortality; however, with early and appropriate intervention, survival rates are excellent.
Normal thermoregulation involves a complex system of interaction between the central nervous system, the cardiovascular system and the skin. Core body temperature, governed by the hypothalamus, depends on the basal metabolic rate and heat transfer to and from the external environment. Heat stress induces cutaneous vasodilation, increasing skin blood flow up to 8L/min, allowing enhanced dissipation of heat.
This is accompanied by a systemic, acute-phase response aiding both tissue repair and modulation of local and systemic inflammation, and is manifested by increased production of cytokines including TNFα, IL-6, IL-8, IL-10. Simultaneously, there is increased transcription and expression of heat-shock proteins that are essential to cellular tolerance of heat stress.
<blockquote> <div> <p class=”QUOTEtextalignedrightMIstyles”>EHS is a leading cause of morbidity and mortality in young athletes, with a peak incidence in the summer months and an under-recognition of its importance by many endurance athletes
Failure of thermoregulation occurs in the setting of severe water and salt depletion due to inability to increase the cardiac output to the required thresholds to dissipate heat peripherally. Cutaneous vasodilatation leads to diversion of blood from visceral organs, and, in this setting, may induce hepatocellular, gut and renal ischaemia, potentiating the systemic inflammatory cascade. In animal models, heatstroke is associated with endotoxaemia due to gut hyper-permeability, which leads to hypotension and increased mortality. There may also be a failure to increase heat-shock protein expression, particularly in the more elderly or un-acclimatised. Non-environmental risk factors for EHS include dehydration, obesity, lack of fitness, medications such as diuretics, caffeine and others that interfere with the normal cardiovascular physiological response, clothing barriers to evaporation and pre-existing medical conditions, particularly cardiovascular disease.
Environmental risk factors include air temperature, air motion and humidity, which can be amplified in those not acclimatised to warm conditions. Acclimatisation occurs over several days to weeks, with repeated exertions in warm conditions, resulting in a protective physiological conditioning with increased plasma volume, increased ability to sweat, enhanced cardiac performance, alterations in the renin-angiotensin-aldosterone system to enhance salt preservation, and enhanced expression of heat-shock proteins.
When heatstroke is suspected, initiation of rapid cooling is the most critical step to avoid catastrophic complications and fatality. Initial measures include removal of clothing and transfer to a cool, shaded environment. External cooling methods produce rapid cooling by use of evaporative heat loss, induced by spraying cool mist on the skin in combination with fanning warm air on the patient or cold-water (1-15°C) immersion.
Cooling blankets or water dousing in conjunction with ice packs to the body, particularly in areas close to major blood vessels such as the axilla, groin and neck, can be considered if immersion is unavailable.
Internal cooling produces more rapid cooling, and can be accomplished with bladder or gastric cool-water lavage, or, rarely, invasive peritoneal or thoracic lavage. Cold-water immersion is favoured as the first-line treatment, with demonstrated efficacy and safety in EHS cohorts, although potential complications such as peripheral vasoconstriction exist.
Other supportive care involves fluid and electrolyte repletion, airway management and close observation for evidence of multi-organ failure. Current evidence does not support routine use of medications such as dantrolene in the initial management of EHS.
Due to the unnecessary mortality associated with EHS, there has been increased focus on preventative measures in sports medicine. Guidelines recognise individual-level preventative measures such as planning the duration and timing of exercise, allowance of rest breaks, appropriate acclimatisation, ensuring adequate fluid and salt replacement with guidance by pre- and post-exercise weight and minimisation of heavy clothing. Organisational level factors include pre-participation medical screening and ensuring availability of on-site medical care and equipment such as rectal thermometers and immersion equipment. Environmental thermal indices such as the wet bulb globe temperature (WGBT) are useful to risk-assess the likelihood of heat-related illnesses and could be used to decide when to cancel endurance events in “unexpected” hot conditions. It appears some trainers, despite adequate knowledge, are reluctant to initiate recommended strategies for a variety of reasons, including lack of initiative, lack of resources and fears of liability.
In conclusion, EHS is a medical emergency with the potential for catastrophic outcomes. Increased use of preventative measures, coupled with prompt recognition and treatment in suspected cases, should lead to a reduction in EHS incidence and mortality.
<div style=”background: #e8edf0; padding: 10px 15px; margin-bottom: 15px;”> <h3>Case report 1</h3>
A healthy 39-year-old female marathoner had a transient loss of consciousness after 23 miles, without witnessed seizure activity. The patient was confused and disorientated at the scene, with a core temperature of 40.5°C. On arrival to the emergency department (ED), the patient had a Glasgow Coma Scale (GCS) of 12/15, temperature of 39.8°C, pulse rate of 140bpm and blood pressure reading of 85/40mmHg without any focal neurological deficit. With rapid cooling measures by ice packs and cooling blankets, her temperature resolved to 36.4°C within 45 minutes and the GCS returned to 15. Initial ECG demonstrated a left bundle branch block (LBBB) and serial high-sensitive troponin measurements peaked at 558ng/L (normal range <14ng/L). The patient admitted to prophylactic NSAID use at the beginning of the race. There was an acute kidney injury (AKI) with peak serum creatinine of 207umol/L, myoglobinuria and a peak creatine kinase (CK) level of 15,997U/L. Initial serum lactate was elevated at 7.0mmol/L. These parameters resolved with aggressive fluid resuscitation.
An echocardiogram showed a structurally normal heart with no regional wall motion abnormalities and the LBBB later completely resolved.
<div style=”background: #e8edf0; padding: 10px 15px; margin-bottom: 15px;”> <h3>Case report 2</h3>
A healthy 32-year-old male marathoner had a generalised seizure after 15 miles, with a recorded core temperature at the scene of 41°C. On arrival to ED, following ice pack cooling measures by paramedics, GCS was 15, with a temperature of 36°C and no haemodynamic instability. Again, there had been prophylactic NSAID use. There was an AKI with a peak serum creatinine of 200umol/L, myoglobinuria and a peak CK level of 23,159U/L, all of which resolved with aggressive fluid resuscitation. There was also evidence of an acute liver injury with a prothrombin time of 21.5s (INR 1.96), albumin 28g/L, peak ALT of 5,628U/L and associated hypoglycaemia. This required infusion of N-acetyl cysteine and dextrose and subsequently fully resolved. An MRI brain scan and electroencephalogram demonstrated no abnormality. The patient was discharged well four days later.
<div style=”background: #e8edf0; padding: 10px 15px; margin-bottom: 15px;”> <h3>Case report 3</h3>
A healthy 29-year-old male marathoner was found agitated and delirious on concealed ground adjacent to the 23-mile course mark, after an estimated 45-to-60 minute unwitnessed ground lie. His initial recorded temperature in the ED was 39.8°C, with cooling measures ongoing by paramedics. On arrival, his GCS was 8/15, with a sinus tachycardia and blood pressure of 100/76mmHg. He was incoherent and agitated and thought to be possibly in a postictal state. He later had a generalised seizure requiring intravenous anticonvulsants, with subsequent sedation and mechanical ventilation. CT brain imaging was unremarkable. There was severe rhabdomyolysis, evidenced by oliguric AKI with initial serum creatinine of 243umol/L, myoglobinuria and a peak CK level of 143,786U/L.
Continuous haemofiltration was commenced for progressive azotaemia, acidosis and anuria. There was also evidence of an acute liver injury with a peak prothrombin time of 24s (INR 2.2) and ALT of 4,815U/L, prompting N-acetyl cysteine infusion until parameters had normalised. The patient was extubated after 24 hours without any evidence of a neurological deficit. Widespread muscular haematomas and ecchymosis later ensued. Intermittent haemodialysis continued following discharge. The patient recovered sufficient renal function after four weeks to discontinue dialysis and returned to a normal serum creatinine at his last review.
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