Severe heat stroke in an experienced athlete

Lee, Richard; Bishop, Gillian; Ashton, Christopher

doi:10.5694/j.1326-5377.1990.tb136802.x

Cited by 16 publications

(3 citation statements)

References 13 publications

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“…The same individual who can tolerate the work and heat load on one occasion may suffer HS due to heat sepsis on another occasion under the same conditions when immune functions and/or gut health are compromised. This concept of transient heat tolerance in the sepsis pathway is illustrated in Figure 1 and may explain the occurrence of HS in people who are well-trained and when performing activities that were well-tolerated before [ 34 , 38 ]. Besides exercise-induced immune suppression, immune functions can also be compromised under other circumstances such as the existence of a sub-clinical infection, recent illness, and prolonged periods of psychological stress, poor nutrition, and sleep deprivation [ 113 , 114 , 115 , 116 ].…”

Section: The Dual Pathway Model Of Heat Strokementioning

confidence: 99%

“…Although heat acclimatization is effective in enhancing thermoregulation, the translation of improvements in thermoregulation to the prevention of HS remains debatable [ 30 , 31 , 32 , 33 , 34 ]. On the contrary, there are multiple reports of trained soldiers, outdoor laborers, and athletes who succumbed to HS [ 34 , 35 , 36 , 37 , 38 , 39 ], which suggests a dissociation between thermoregulation and heat tolerance. Two studies that administered continuous core temperature (Tc) measurement in well-acclimatized half-marathon runners showed that peak Tc in 30% to 40% of the runners were >40 °C (highest recorded was 41.7 °C) in the absence of heat injury or compromise in wellness [ 28 , 40 ].…”

Section: Introductionmentioning

confidence: 99%

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Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease

Lim

2018

Antioxidants

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Heat stroke (HS) is an ancient illness dating back more than 2000 years and continues to be a health threat and to cause fatality during physical exertion, especially in military personnel, fire-fighters, athletes, and outdoor laborers. The current paradigm in the pathophysiology and prevention of HS focuses predominantly on heat as the primary trigger and driver of HS, which has not changed significantly for centuries. However, pathological and clinical reports from HS victims and research evidence from animal and human studies support the notion that heat alone does not fully explain the pathophysiology of HS and that HS may also be triggered and driven by heat- and exercise-induced endotoxemia. Exposure to heat and exercise stresses independently promote the translocation of lipopolysaccharides (LPS) from gram-negative bacteria in the gut to blood in the circulatory system. Blood concentration of LPS can increase to a threshold that triggers the systemic inflammatory response, leading to the downstream ramifications of cellular and organ damage with sepsis as the end point i.e., heat sepsis. The dual pathway model (DPM) of HS proposed that HS is triggered by two independent pathways sequentially along the core temperature continuum of >40 °C. HS is triggered by heat sepsis at Tc < 42 °C and by the heat toxicity at Tc > 42 °C, where the direct effects of heat alone can cause cellular and organ damage. Therefore, heat sepsis precedes heat toxicity in the pathophysiology of HS.

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Section: The Dual Pathway Model Of Heat Strokementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heat Sepsis Precedes Heat Toxicity in the Pathophysiology of Heat Stroke—A New Paradigm on an Ancient Disease

Lim

2018

Antioxidants

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“…Their water is absorbed as fast as plain water, and they offer sugar for energy and also some sodium. 4) Monitor weight. Weigh nude before and after each session.…”

Section: Treating Heat Illnessmentioning

confidence: 99%

Treatment of Suspected Heat Illness

1998

Int J Sports Med

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1. Despite advances in the art and science of fluid balance, exertional heat illness -- even life-threatening heat stroke -- remains a threat for some athletes today. 2. Risk factors for heat illness include: being unacclimatized, unfit, or hypohydrated; certain illnesses or drugs; not drinking in long events; and a fast finishing pace. 3. Heat cramps typically occur in conditioned athletes who compete for hours in the sun. They can be prevented by increasing dietary salt and staying hydrated. 4. Early diagnosis of heat exhaustion can be vital. Early warning signs include: flushed face, hyperventilation, headache, dizziness, nausea, tingling arms, piloerection, chilliness, incoordination, and confusion. 5. Pitfalls in the diagnosis of heat illness include: confusion preventing self-diagnosis; the lack of trained spotters; rectal temperature not taken promptly; the problem of "seek not, find not;" and the mimicry of heat illness. 6. Heat stroke is a medical emergency. Mainstays of therapy include: emergency on-site cooling; intravenous fluids; treating hypoglycemia as needed; intravenous diazepam for seizures or severe cramping or shivering; and hospitalizing if response is slow or atypical. 7. The best treatment is prevention. Tips to avoiding heat illness include: rely not on thirst; drink on schedule; favor sports drinks; monitor weight; watch urine; shun caffeine and alcohol; key on meals for fluids and salt; stay cool when you can; and know the early warning signs of heat illness.

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