The Gastrointestinal Exertional Heat Stroke Paradigm: Pathophysiology, Assessment, Severity, Aetiology and Nutritional Countermeasures.

Exertional heat stroke (EHS) is a life-threatening medical condition involving thermoregulatory failure and is the most severe condition along a continuum of heat-related illnesses. Current EHS policy guidance principally advocates a thermoregulatory management approach, despite growing recognition that gastrointestinal (GI) microbial translocation contributes to disease pathophysiology. Contemporary research has focused to understand the relevance of GI barrier integrity and strategies to maintain it during periods of exertional-heat stress. GI barrier integrity can be assessed non-invasively using a variety of in vivo techniques, including active inert mixed-weight molecular probe recovery tests and passive biomarkers indicative of GI structural integrity loss or microbial translocation. Strenuous exercise is strongly characterised to disrupt GI barrier integrity, and aspects of this response correlate with the corresponding magnitude of thermal strain. The aetiology of GI barrier integrity loss following exertional-heat stress is poorly understood, though may directly relate to localised hyperthermia, splanchnic hypoperfusion-mediated ischemic injury, and neuroendocrine-immune alterations. Nutritional countermeasures to maintain GI barrier integrity following exertional-heat stress provide a promising approach to mitigate EHS. The focus of this review is to evaluate: (1) the GI paradigm of exertional heat stroke; (2) techniques to assess GI barrier integrity; (3) typical GI barrier integrity responses to exertional-heat stress; (4) the aetiology of GI barrier integrity loss following exertional-heat stress; and (5) nutritional countermeasures to maintain GI barrier integrity in response to exertional-heat stress.

Bacterial translocation in heat stroke.

The scientific community is fully aware of the importance of heat-related illness and heat stroke syndrome. Numerous guidelines have been recently published and most of them agree on the key role played by the intestine. Likewise, the role of endotoxinemia in the pathophysiology is well established. However, the possibility of bacterial translocation is not mentioned. Our patient illustrates the likelihood of bacterial translocation in heat stroke and consistently the potential need of antibiotic therapy. A 45-year-old man diagnosed with paranoid schizophrenia was confined in a penitentiary center. One summer day in which a temperature of 41 degrees C was observed in the shade, the patient was found in deep coma with an axillary temperature of 42 degrees C. Multiorgan failure was detected in the hospital. Other causes of coma and/or hyperthermia were excluded, and heat stroke was diagnosed. Blood cultures were positive for Pseudomonas aeruginosa and Escherichia coli. Infection site was not identified despite of an exhaustive search. The patient fully recovered after 48 hours. On the basis of review of the literature, we think that bacterial translocation can take part in the pathophysiology of heat stroke. Therefore, antibiotic treatment must be evaluated in heat stroke patients.