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“Tell me, what is it you plan to do, with your one wild and precious life?”
When carbon dioxide retention tickles intensivists’ neurons, clusters of adjacent synapses spark in deep sulci – discharging neural silos of respiratory physiology, alveolar ventilation, pH interpretation and the like. But like flash-bulbs against shadowy storm clouds in the distance, rising carbon dioxide should electrify a global perspective upon our collective cognitive canvas. With no clear atmospheric BiPAP on the horizon, the waxing responsibility of severe weather in human sickness is revealed. Yes, heat-related illness is, and will be, frequently faced by clinicians within the inhospitable vortices of climate change and acute care medicine.
General symptoms and signs
Many of the symptoms and signs of heat-related illness fall from the hemodynamic aberrations described previously. With blood volume shifted away from the gut, brain and kidneys as a convective compensatory mechanism, it is unsurprising that non-specific gastrointestinal and neurological symptoms are harbingers of heat-associated illness. Nausea, vomiting, fatigue, malaise, dizziness and visual disturbances typify a patient in whom excessive heat energy is accumulating. As cerebral blood flow falls during heat stress, heat syncope can occur especially when a large fraction of blood volume is diverted to the skin coupled with orthostatic stress. Additional signs include confusion, and tachycardia. With diminished renal perfusion, oligoanuria may be present.
Heat exhaustion most often presents with a core temperature between 37 and 40 degrees C [i.e., 98.6 to 104 F]. The symptoms of heat exhaustion are more subdued than heatstroke and rapidly resolve with rehydration and cooling. Importantly, any significant and non-transient [i.e., > 20-30 minutes] central nervous system dysfunction should lead the clinician towards a heatstroke diagnosis, as elaborate upon below. Heat exhaustion may present concurrently with significant hyponatremia, especially if the patient was overzealous with free water intake. With significant hyponatremia, central nervous system signs and symptoms such as confusion and even seizures can present with heat exhaustion and this may be mistaken for heatstroke. The approach to acute sodium/free water abnormality may be found elsewhere.
Heatstroke is a medical emergency and it has two crucial diagnostic elements:
- Disturbed central nervous function
While not universal, core temperature is typically between 40 and 44 degrees C with reports up to 47 degrees C [i.e., 117 F!]. Parenthetically, in human volunteer studies, the thermal maximum [i.e., the temperature and duration to which human cells may be exposed prior to damage] is estimated to be 42 degrees C for 45 minutes to 8 hours. Crucially, however, consensus statements endorse limiting extreme hyperthermia [i.e., > 40.5 degrees Celsisus] to less than 30 minutes. The characteristic central nervous manifestations of heatstroke are confusion, irritability, ataxia and, potentially, seizures and coma.
Heatstroke is often dichotomized into ‘classic’ and ‘exertional’ subtypes with the former typically evolving as a consequence of environmental exposure, for example during heat waves. For this reason, classic heatstroke is sometimes referred to as ‘passive.’ With respect to the heat transfer equation, classic heatstroke progresses when the normal compensatory mechanisms for heat liberation [e.g., dry and evaporative transfer] are overwhelmed. Thus, S is > zero and heat energy is stored within the body, typically over an exposure period over many days. Because the elderly and in those with chronic disease are predisposed to aberrant hemodynamics – and therefore inferior convective and evaporative heat loss – classic heatstroke is often encountered in patients with these diatheses. For example, the odds ratio for risk of death during a heat wave is 6.44 for those confined to bed and 3.35 for those who do not leave home daily. While it is generally taught that heatstroke presents with a core temperature above 40 degrees Celsius [i.e., 104 degrees Fahrenheit], classic heatstroke may present with minimal core temperature elevation.
By contrast, exertional heatstroke develops sporadically in relatively young and healthy individuals when excessive metabolic heat overwhelms heat liberation mechanisms; it usually presents acutely over hours with high core temperature, but may develop in less than one hour. Exertional heat stroke can also strike individuals participating in psychedelic-trance music festivals as drugs such as amphetamines of MDMA accentuate metabolic heat liberation during dancing. Unlike classic or passive heatstroke, the mortality rate in the exertional subtype is estimated at less than 5%.
The differential diagnosis of hyperthermia and mental status change is relatively limited to infection [e.g., bacteremia] and toxic misadventures [e.g., neuroleptic malignant syndrome, anticholinergic poisoning, serotonin syndrome, topiramate etc.], though other primary central nervous system insults are also possible.
Core temperature, especially in heatstroke, should be monitored via the rectum, bladder, esophagus or pulmonary artery catheter. Peripheral temperature readings may underestimate core temperature by 1 degree C and emergent cooling can exaggerate peripheral error. Nevertheless, monitoring skin temperature is informative as vasoconstriction of the cutaneous vascular beds occurs around 30 degrees C. Therefore, skin temperature below this threshold presents a risk for heat retention and may herald the onset of shivering.
Beyond temperature, and especially in heatstroke, additional attention must be paid to vital signs, cardiorespiratory function, electrolytes, hepatic function, creatine phosphokinase and the coagulation cascade.
In patients with classic heatstroke, 60% presented with mixed metabolic acidosis and respiratory alkalosis, whereas in exertional heatstroke metabolic acidosis predominates. Similarly, exertional heatstroke tends to present with more significant creatine phosphokinase elevation and electrolyte disturbances such as hyperkalemia, hyperphosphatemia, hypocalcemia and creatinine elevation. One-third of exertional heatstroke had AKI. As well, patients with heatstroke remain at increased risk for hepatic failure, disseminated coagulation and thromboses even days after cooling. There is a well-documented heatstroke-related inflammatory response that mirrors the systemic inflammatory response syndrome. Thus, similar to septic shock, multi-organ failure is a well-known complication of heatstroke.
With the above, discursive briefing on heat-related illness, the next and final section presents a perfunctory view of therapy for both heat exhaustion and heatstroke.