scholarly journals Exertional Heat Stroke in Athletes

2013 ◽  
Vol 1 (1) ◽  
pp. 135-139
Author(s):  
Metodija Kjertakov ◽  
Yoram Epstein

Exercising in hot and especially humid environment can cause rise in body core temperature to such a critical level that it does not only reduce performance, but also may ultimately lead to exertional heat stroke (EHS). This illness is true medical emergency that can result in significant morbidity and mortality, if not early recognized and promptly treated. Diagnostic criteria for EHS are body core temperature above 40ºC and central nerve system dysfunction. Any athlete experiencing such symptoms should be immediately exposed to aggressive cooling treatment aimed to lower the elevated core temperature to near normal as quickly as possible. Ice water immersion is highly recommended as a cooling method because it provides the fastest cooling rates and is associated with lowest mortality rates. Athletes cooled rapidly soon after the onset of EHS usually recover without complications and are able to return to normal training in hot environment within a few weeks. EHS is also a preventable condition, and its occurrence can be minimized by implementing a few simple measures.

2019 ◽  
Vol 127 (5) ◽  
pp. 1338-1348 ◽  
Author(s):  
Orlando Laitano ◽  
Lisa R. Leon ◽  
William O. Roberts ◽  
Michael N. Sawka

During the past several decades, the incidence of exertional heat stroke (EHS) has increased dramatically. Despite an improved understanding of this syndrome, numerous controversies still exist within the scientific and health professions regarding diagnosis, pathophysiology, risk factors, treatment, and return to physical activity. This review examines the following eight controversies: 1) reliance on core temperature for diagnosing and assessing severity of EHS; 2) hypothalamic damage induces heat stroke and this mediates “thermoregulatory failure” during the immediate recovery period; 3) EHS is a predictable condition primarily resulting from overwhelming heat stress; 4) heat-induced endotoxemia mediates systemic inflammatory response syndrome in all EHS cases; 5) nonsteroidal anti-inflammatory drugs for EHS prevention; 6) EHS shares similar mechanisms with malignant hyperthermia; 7) cooling to a specific body core temperature during treatment for EHS; and 8) return to physical activity based on physiological responses to a single-exercise heat tolerance test. In this review, we present and discuss the origins and the evidence for each controversy and propose next steps to resolve the misconception.


1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643 Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome. ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA


2017 ◽  
Vol 26 (5) ◽  
pp. 447-451 ◽  
Author(s):  
Tyler T. Truxton ◽  
Kevin C. Miller

Clinical Scenario:Exertional heat stroke (EHS) is a medical emergency which, if left untreated, can result in death. The standard of care for EHS patients includes confirmation of hyperthermia via rectal temperature (Trec) and then immediate cold-water immersion (CWI). While CWI is the fastest way to reduce Trec, it may be difficult to lower and maintain water bath temperature in the recommended ranges (1.7°C–15°C [35°F–59°F]) because of limited access to ice and/or the bath being exposed to high ambient temperatures for long periods of time. Determining if Trec cooling rates are acceptable (ie, >0.08°C/min) when significantly hyperthermic humans are immersed in temperate water (ie, ≥20°C [68°F]) has applications for how EHS patients are treated in the field.Clinical Question:Are Trec cooling rates acceptable (≥0.08°C/min) when significantly hyperthermic humans are immersed in temperate water?Summary of Findings:Trec cooling rates of hyperthermic humans immersed in temperate water (≥20°C [68°F]) ranged from 0.06°C/min to 0.19°C/min. The average Trec cooling rate for all examined studies was 0.11±0.06°C/min.Clinical Bottom Line:Temperature water immersion (TWI) provides acceptable (ie, >0.08°C/min) Trec cooling rates for hyperthermic humans post-exercise. However, CWI cooling rates are higher and should be used if feasible (eg, access to ice, shaded treatment areas).Strength of Recommendation:The majority of evidence (eg, Level 2 studies with PEDro scores ≥5) suggests TWI provides acceptable, though not ideal, Trec cooling. If possible, CWI should be used instead of TWI in EHS scenarios.


2017 ◽  
Vol 14 (9) ◽  
pp. 703-711 ◽  
Author(s):  
Dallon T. Lamarche ◽  
Robert D. Meade ◽  
Andrew W. D'Souza ◽  
Andreas D. Flouris ◽  
Stephen G. Hardcastle ◽  
...  

2008 ◽  
Vol 294 (2) ◽  
pp. F309-F315 ◽  
Author(s):  
Joo Lee Cham ◽  
Emilio Badoer

Redistribution of blood from the viscera to the peripheral vasculature is the major cardiovascular response designed to restore thermoregulatory homeostasis after an elevation in body core temperature. In this study, we investigated the role of the hypothalamic paraventricular nucleus (PVN) in the reflex decrease in renal blood flow that is induced by hyperthermia, as this brain region is known to play a key role in renal function and may contribute to the central pathways underlying thermoregulatory responses. In anesthetized rats, blood pressure, heart rate, renal blood flow, and tail skin temperature were recorded in response to elevating body core temperature. In the control group, saline was microinjected bilaterally into the PVN; in the second group, muscimol (1 nmol in 100 nl per side) was microinjected to inhibit neuronal activity in the PVN; and in a third group, muscimol was microinjected outside the PVN. Compared with control, microinjection of muscimol into the PVN did not significantly affect the blood pressure or heart rate responses. However, the normal reflex reduction in renal blood flow observed in response to hyperthermia in the control group (∼70% from a resting level of 11.5 ml/min) was abolished by the microinjection of muscimol into the PVN (maximum reduction of 8% from a resting of 9.1 ml/min). This effect was specific to the PVN since microinjection of muscimol outside the PVN did not prevent the normal renal blood flow response. The data suggest that the PVN plays an essential role in the reflex decrease in renal blood flow elicited by hyperthermia.


2002 ◽  
Vol 80 (3) ◽  
pp. 226-232 ◽  
Author(s):  
Frédéric Canini ◽  
Nadine Simler ◽  
Lionel Bourdon

The effects of MK801 (dizocilpine), a glutamate NMDA receptor antagonist, on thermoregulation in the heat were studied in awake rats exposed to 40°C ambient temperature until their body core temperature reached 43°C. Under these conditions, MK801-treated rats exhibited enhanced locomotor activity and a steady rise in body core temperature, which reduced the heat exposure duration required to reach 43°C. Since MK801-treated rats also showed increased striatal dopaminergic metabolism at thermoneutrality, the role of dopamine in the MK801-induced impairment of thermoregulation in the heat was determined using co-treatment with SCH23390, a dopamine D1 receptor antagonist. SCH23390 normalized the locomotor activity in the heat without any effect on the heat exposure duration. These results suggest that the MK801-induced impairment of thermoregulation in the heat is related to neither a dopamine metabolism alteration nor a locomotor activity enhancement.Key words: heatstroke, NMDA receptor, thermoregulation, dopamine, locomotion.


2013 ◽  
Vol 84 (11) ◽  
pp. 1153-1158 ◽  
Author(s):  
Jayme D. Limbaugh ◽  
Gregory S. Wimer ◽  
Lynn H. Long ◽  
William H. Baird

2015 ◽  
Vol 4 (S1) ◽  
Author(s):  
Yoram Epstein ◽  
Savyon Mazgaoker ◽  
Doron Gruber ◽  
Daniel S Moran ◽  
Ran Yanovich ◽  
...  

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