Exertional Heat Illness / Heat Stroke

Exertional heat stroke is not a random misfortune, and an examiner asking "how would you have prevented this?" is asking for these. The dominant modifiable factor is acclimatisation state: the great majority of cases cluster in the first days of a preseason, training camp or military intake, before physiological adaptation has occurred. Acclimatisation takes roughly ten to fourteen days of progressive exposure, over which plasma volume expands, sweating begins earlier and at a higher rate, and sweat sodium falls - which is why an athlete returning from a break, or arriving from a cooler climate, is at risk even though they are fit.

The remaining factors group usefully:

• Environmental - high ambient temperature and humidity, since it is evaporation that does the cooling; this is why the wet-bulb globe temperature (WBGT), which combines temperature, humidity, radiant heat and wind, governs heat policies rather than the air temperature alone. Still air and full sun add further load.
• Equipment and clothing - occlusive kit is a major and often overlooked contributor. American football pads and helmet, body armour and full protective clothing prevent evaporation over much of the body surface, and helmet removal is part of the initial management.
• Individual - poor aerobic fitness, high body mass and adiposity, a recent febrile or gastrointestinal illness, sleep deprivation, dehydration at the start, and certain medications and supplements (stimulants, anticholinergics, some diuretics).
• A previous episode of exertional heat stroke, which confers an increased risk of a further one and is the reason recurrent cases warrant a search for an underlying myopathy or an inherent heat intolerance.
• Sickle cell trait, which is a risk factor for exertional collapse and rhabdomyolysis rather than for hyperthermia specifically, but shares the same high-intensity, unacclimatised setting.
• Motivation and supervision - the culture that rewards pushing through, and the absence of a mandated work-to-rest ratio, are why events and military selection produce clusters.

"Treat as heat stroke until proven otherwise" still requires a deliberate differential, because the dangerous mimic - exercise-associated hyponatraemia - needs the OPPOSITE fluid management.

Enough about hyponatraemia to act on it

Because the two conditions are managed in opposite directions, a few specifics are worth carrying rather than looking up. Exercise-associated hyponatraemia arises from drinking more fluid than is lost, typically in slower participants in long events who take on water at every station; the giveaway on history is that the athlete has gained weight during the event rather than lost it. Symptoms track the sodium: nausea, headache and bloating at mild levels, progressing to confusion, seizures and respiratory arrest from cerebral and pulmonary oedema as it falls further.

The management rule is the one to remember. Do not give hypotonic fluid, and do not give volume for "dehydration" in a collapsed athlete until the sodium is known - in EAH that is precisely what precipitates the fatal cerebral oedema, and the reflex to run in a litre of saline is the error that kills. Symptomatic hyponatraemia is treated with a small bolus of hypertonic (3%) saline, repeated as needed to reverse the neurological signs, which is deliberately a small volume of very salty fluid rather than a large volume of slightly salty fluid. An athlete who is merely uncomfortable with a suspected mild case is managed by fluid restriction and observation, not by drinking more.

"Cool first, transport second" is only safe if cooling is done correctly, measured correctly and stopped correctly.

What does not work, and what makes it worse

Two drug reflexes have to be actively suppressed, and both are popular wrong answers.

Antipyretics do nothing in heat stroke. Paracetamol, aspirin and NSAIDs work by lowering a hypothalamic set point that has been raised by pyrogens. In exertional heat stroke the set point is normal - the problem is that heat production has overwhelmed dissipation - so there is no set point to lower and no antipyretic effect to be had. Worse, they are actively unhelpful in this specific patient: paracetamol is hepatotoxic in an athlete whose liver is about to be injured, and NSAIDs are nephrotoxic and antiplatelet in one who is heading for acute kidney injury and coagulopathy. Dantrolene likewise has no established role, because this is not malignant hyperthermia - the pathophysiology is environmental and exertional heat load, not a ryanodine-receptor defect (contrast with Malignant Hyperthermia).

The other error is fluid by reflex. Cooling, not volume, is the resuscitation here, and until the sodium is known a large-volume hypotonic infusion risks converting a survivable collapse into fatal cerebral oedema if the diagnosis is actually exercise-associated hyponatraemia.

The complications do not all appear at once

Successful cooling on the field is the decisive intervention, but it is not the end of the illness, and the timing matters because the athlete who looks well at two hours can deteriorate later.

• Immediately - seizures, arrhythmia, aspiration and the consequences of a fall or collapse.
• Over the first 24 hours - rhabdomyolysis with hyperkalaemia and myoglobinuric acute kidney injury, best anticipated with creatine kinase, potassium, renal function and urine output rather than waited for.
• At 24 to 72 hours - hepatic injury, which characteristically peaks late; a small number progress to fulminant liver failure requiring transplantation. This is the complication most likely to be missed by an early discharge, and it is the reason a genuine exertional heat stroke is admitted and re-checked rather than sent home once cool and lucid.
• Also - disseminated intravascular coagulation, acute respiratory distress syndrome, and persisting neurological deficit, most often cerebellar, in those cooled slowly.

Prevention that is specific enough to implement

"Acclimatise, hydrate and monitor WBGT" is only useful if it names what to do. A workable heat plan means graduated acclimatisation over ten to fourteen days, with equipment introduced progressively rather than from day one; activity modified against WBGT thresholds with defined work-to-rest ratios and mandated fluid breaks; and, decisively, an immersion tub filled and on site before the session starts, because a policy that requires someone to fetch ice after the collapse has already lost the golden half-hour. The written emergency action plan should name who takes the rectal temperature, who starts immersion and who calls the ambulance, and it should be rehearsed. Sessions should also be structured so that an athlete can stop without penalty - the cultural point does more work than any of the physiological ones.

Return to play

Return is graded and unhurried, and the principle is that the athlete does not restart until the organ injury has resolved and heat tolerance has been demonstrated.

• Rest from exercise until symptom-free with normalised laboratory markers - creatine kinase, renal and liver function - which commonly takes at least a week and sometimes considerably longer.
• Graded reintroduction over subsequent weeks: light activity in a cool environment first, then increasing intensity, then increasing heat exposure, then full equipment - changing one variable at a time so that a failure identifies itself.
• Heat tolerance testing at around six weeks or more is used where recovery is slow, where the episode was severe, or before returning to a high-risk occupational setting; military services in particular use a standardised exercise-in-heat protocol to document tolerance before full clearance.
• A recurrent episode should prompt a search for a predisposing cause - an underlying myopathy, a malignant-hyperthermia-related susceptibility, or a persisting intolerance - and a frank reconsideration of the athlete's participation in the setting that caused it.