The impact of allergic rhinitis on functional, aesthetic and scar outcomes after open septorhinoplasty: a prospective controlled study.

The anticipated rise in global temperature in the 21 century will likely increase the risk of heat illness, which in its severest form can be fatal (). Accordingly, there is a growing need to advance current knowledge of heat illness etiology and to develop mitigation strategies to reduce heat illness prevalence. Heat illness is commonly classified as either classical or exertional (EHI). Classical heat illness predominantly occurs in older individuals, who often have comorbidities, during passive exposure to hot environmental conditions (). EHI typically occurs in young and seemingly healthy individuals (e.g., military personnel and athletes) during strenuous physical activity in both cool and hot environmental conditions (,). EHI is considered to occur on a severity spectrum from mild (i.e., heat exhaustion) to severe (i.e., heat stroke). Common signs and symptoms of mild EHI include headache, nausea, and dizziness (). Central nervous system disturbance is the defining feature of severe EHI, typically accompanied by hyperthermia and evidence of end-organ damage in the days following the episode (). Widely reported risk factors for EHI include low aerobic fitness, an elevated wet bulb globe temperature (WBGT), hypohydration, and high motivation (). Unfortunately, much of the underpinning evidence outlining EHI risk factors is derived from retrospective clinical case reviews, which lack objective measures and comparator controls (–). Furthermore, widely reported risk factors for EHI are absent in many cases, pointing to the involvement of alternative risk factors in the development of a significant number of EHI cases (,). Expert statements highlight ongoing infection as a likely predisposing EHI risk factor, but empirical evidence in humans is equivocal (,). Experimental evidence examining the pathogenesis of EHI in rodents supports the proposition that infection and associated inflammation increase EHI risk (–). For example, exogenous administration of viral or bacterial mimics or an inflammatory stimulant during heat stress can increase deep body temperature and elevate both the likelihood and severity of heat stroke in rodents (–). In humans, a case study of an individual suffering from a bacterial infection showed increased heat strain both at rest and during exercise-heat stress (). Other case studies have proposed that recent infection was a contributing factor for exertional heat stroke in a single well-trained runner during a marathon () and in three of six EHI fatalities in the Israeli Defense Forces (). However, clinical reviews of military EHI cases present a mixed picture regarding a role for recent or ongoing infection in EHI etiology. One examination of US military clinical records showed that respiratory infection in the preceding week increased the risk of both mild and severe EHI (). Whereas other analyses of US and U.K. military clinical records conclude that “prior illness” or “intercurrent febrile or infectious illness” did not increase severe EHI risk (,). Unfortunately, these clinical case reviews are limited by a lack of objective measures (e.g., for respiratory infection and EHI) and comparator controls: individuals who complete the same exercise but do not experience EHI. As such, a conclusion about the influence of respiratory infection on EHI susceptibility cannot be reached until prospective cohort studies are completed that include the requisite controls, objective assessments for both respiratory infection and EHI, and statistical analyses that account for other widely considered EHI risk factors. The aim of this prospective cohort study was to examine the association between respiratory infection and EHI in military recruits undertaking strenuous physical activity. It was hypothesized that respiratory infection would be associated with increased EHI susceptibility.