1. 热射病的基础概念与冬季特殊性界定
1.1 热射病的核心定义与分类
热射病是一种危及生命的严重热相关疾病，其核心特征为核心体温升高至40°C以上，并伴有中枢神经系统功能障碍，如谵妄、抽搐、共济失调甚至昏迷等 12345。这种体温升高是由于机体产热和散热失衡所致 67。
根据其发生原因，热射病通常可分为两类：
- 经典型热射病（Classic Heatstroke, CHS）：主要由被动暴露于高温环境引起，常见于年老体弱、慢性病患者或婴幼儿，通常发生在夏季热浪期间 238。这类患者的体温调节系统可能因疾病或年龄而受损，对环境热负荷的适应能力较差。
- 劳力型热射病（Exertional Heatstroke, EHS）：主要由剧烈体力活动导致自身产热过高引起，即使在非极端高温环境下也可能发生 238。劳力型热射病多见于年轻健康的个体，例如运动员、士兵或从事重体力劳动者 289。其发病机制涉及剧烈运动导致的大量产热，超过了身体的散热能力，从而使核心体温迅速升高 7。
在冬季，虽然环境温度较低，但热射病仍有发生，且主要以劳力型热射病为主。这是因为在寒冷季节，人们进行剧烈运动（如滑雪、冬季长跑、高强度训练等）时，身体会产生大量热量。如果同时穿着厚重保暖衣物，或在密闭、通风不良的室内环境中运动，将严重阻碍体表散热，导致核心体温持续升高，最终引发劳力型热射病 29。此外，脱水、某些药物使用以及个体易感性等因素也可能增加冬季劳力型热射病的风险 568。因此，在冬季讨论热射病，更需要关注劳力型热射病的特点及其在低温环境下的特殊发病机制。
1.2 冬季热射病的概念延伸
冬季热射病的概念似乎与人们对热射病通常发生在炎热夏季的认知相悖。这种矛盾性源于对“热”的传统理解与生物体热平衡机制的复杂性。热射病的核心在于机体产热与散热的失衡，导致核心体温异常升高，而非简单地由环境温度决定 5。在冬季，环境温度较低，但这并不意味着人体无法产生或积聚过多的热量。
冬季热射病的界定，重点在于明确其发生的特殊场景和机制，以区别于夏季高温下的传统热射病：
场景特殊性：冬季热射病并非指在冰天雪地中直接因环境热暴露导致，而是多发生在以下特定情境中：
- 高强度冬季运动：例如越野滑雪、高山滑雪、冰球、冬季马拉松等剧烈运动。这些活动本身会产生巨大代谢热量，尤其当运动员穿着厚重、不透气的保暖衣物时，可能会限制汗液蒸发，导致热量在体内蓄积。
- 室内过度保暖与活动：在供暖充足的室内环境（如健身房、训练馆、暖气房等），如果进行高强度运动或长时间剧烈体力活动，同时室内通风不良、空气湿度较高，同样会阻碍散热，引发核心体温升高。老年人在室内过度取暖或缺乏有效降温措施，也有发生室内热射病的风险 10。
- 户外作业与特定防护：从事冬季户外重体力劳动者，如建筑工人、军人等，为抵御寒冷可能穿着多层或厚重的防护服。这些服装在提供保暖的同时，也可能限制热量散发，尤其是在劳动强度较大时，容易导致体热蓄积。
发病机制差异化：与夏季热射病主要强调环境热负荷（如气温、湿度、太阳辐射）不同 11，冬季热射病更侧重于内源性产热过剩与散热受阻的矛盾。尽管环境温度低，但厚重衣物、高强度运动、以及可能存在的脱水（在寒冷环境中，口渴感可能不明显，导致补水不足）等因素，共同促成了核心体温的失控性升高。此外，低温环境下血管收缩反应可能在一定程度上影响皮肤散热，进一步加剧了散热困难。
综上，冬季热射病是对传统热射病概念的延伸和细化，它强调了在低温季节特定条件下的热平衡障碍，要求我们重新审视热射病的风险因素和预防策略，尤其是在评估运动强度和着装选择方面。
2. 冬季热射病的流行病学特征分析
2.1 高发场景与人群分布
冬季热射病的流行病学特征与夏季有所不同，其高发场景和易感人群呈现出明显的季节性与活动相关性。尽管冬季气温较低，但特定活动和环境因素仍可导致体内热量过度蓄积，引发热射病。
高发场景主要包括：
- 冬季户外运动场所： 涉及高强度体力活动的冬季运动，如越野滑雪、高山滑雪、单板滑雪、冰球、冰壶以及冬季马拉松等，可能给运动员带来体温调节的挑战 12。在这些运动中，运动员为保持体温或追求运动表现，通常会穿着多层或保暖性强的运动服饰。然而，这些衣物在运动过程中可能限制汗液蒸发，阻碍热量散发，导致核心体温急剧升高。此外，寒冷环境下风速较大，但人体在剧烈运动时仍可能出现过热情况，特别是在高强度间歇训练或长时间耐力运动中。
- 室内过度加热环境中的剧烈活动： 在供暖充足的室内环境，如健身房、体育馆、住宅暖气房等，如果进行高强度运动，尤其是在通风不良或湿度较高的密闭空间，人体散热效能会显著降低。例如，一些运动员为了在短时间内提高体能，可能会在过度加热的室内进行训练，这极大地增加了热射病的风险。老年人在室内过度取暖，且活动量较大时，也可能面临风险。
- 户外作业与特定职业环境： 寒冷地区的户外工作者，如建筑工人、电力检修人员、军事人员等，为抵御严寒通常会穿着厚重、多层的防寒服。当他们从事高强度体力劳动时，身体产热量激增，而厚重的服装会妨碍热量有效散发，导致体热蓄积。消防员在执行任务时，穿着的阻燃防护服能够提供保护，但也显著增加了热负荷和生理应激 1314。长时间穿戴这些服装进行剧烈活动，有可能增加热射病的风险。
易感人群的分布特征：
- 运动员： 极端炎热或寒冷的环境对运动员的训练和比赛都构成挑战，医生应告知教练和运动员相关风险并提供预防和管理措施 15。运动员常常处于体能极限，代谢产热量巨大，且可能因追求成绩而忽视早期过热的信号。运动员在脱水状态下，调节醛固酮和精氨酸加压素的能力会增强，这些激素在维持体液平衡中发挥作用，但脱水本身会增加热应激的风险 16。
- 户外工作者： 从事冬季户外重体力劳动的工人，由于工作强度大和防护服限制散热，易发生热射病。
- 老年慢性病患者： 尽管经典型热射病主要发生在夏季，但冬季在室内过度取暖、缺乏有效降温手段的老年人，特别是伴有心血管疾病、糖尿病、慢性呼吸道疾病等基础疾病的患者，其体温调节功能可能受损，对热应激的耐受性较差，亦是热射病的易感人群。
- 其他个体： 肥胖者、服用某些影响体温调节药物的患者（如抗抑郁药、抗组胺药、利尿剂等）、以及睡眠不足、身体状况不佳的个体，在冬季进行高强度活动时，热射病的风险也会增加。
2.2 时间与地域分布规律
冬季热射病的发生具有特定的时间和地域分布规律，这与气候特征、生活习惯以及人类活动模式密切相关。
时间集中期：
尽管热射病常与夏季高温相联系，但冬季并非完全安全。冬季热射病的时间集中期主要体现在以下几个方面：
- 极端气温波动期： 在冬季，尤其是在季节交替或寒潮来临/离去时，气温可能出现剧烈波动。例如，当气温突然升高或经历一段较暖和的天气后，人们可能未能及时调整着装，或在进行户外活动时低估了身体的产热负荷，从而增加了热射病的风险。
- 供暖初期与持续供暖期： 在北方地区，供暖初期由于室内外温差较大，且室内可能存在过度供暖的情况，如果同时在室内进行剧烈运动或长时间处于密闭空间，体热无法有效散发，易导致热射病的发生。例如，有案例报告指出，即使在冬季，由于电热毯使用不当导致过热，也可能引发致命性热射病 17。同样，在冬季将汽车长时间停放在阳光下并开启暖气，车内温度会迅速升高，可在短时间内达到危及生命的水平，即使在寒冷天气下也可能导致成年人热射病死亡 18。婴儿在密闭车厢内即使在冬季也可能达到危险的热负荷阈值，提示了车内环境对个体体温的影响不容忽视 19。
- 冬季节假日与休闲活动期： 冬季假期，如圣诞节、春节等，是人们进行冬季运动和室内娱乐活动的高峰期。滑雪、冰上运动、长时间室内聚会等活动，如果伴随过度劳累、酒精摄入或补水不足，可能增加热射病发病风险。
地域高发特点：
冬季热射病的地域分布则主要受到地理位置、气候条件和当地生活方式的影响：
- 高纬度/高海拔地区： 这些地区冬季漫长且严寒，人们更倾向于穿着厚重保暖衣物进行户外活动或工作。例如，军事行动在伊拉克和阿富汗等地的冬季，低温是主要的健康威胁，尤其是在阿富汗的山区，强降雪会带来额外的挑战 20。在这种环境下，士兵为保暖穿着的装备，在剧烈体力活动时可能成为散热障碍。此外，高海拔地区空气稀薄，可能影响机体对热应激的生理反应。
- 室内过度取暖普遍的地区： 在寒冷地区，家庭和公共场所普遍使用暖气设备。如果室内温度设置过高，通风不良，同时有人进行剧烈活动，或老年人长时间处于这种环境，都可能导致体温过高。
- 冬季运动盛行地区： 在滑雪胜地、冰雪运动中心等地区，由于冬季运动人口基数大，进行高强度体力活动的人数多，因此这些地区报告冬季热射病病例的可能性也相对较高。
气候与人为因素的协同影响：
冬季热射病的发病往往是气候因素（如气温波动、高湿度等）与人为因素（如室内过度取暖、不当着装、剧烈运动等）协同作用的结果。
- 气候因素： 尽管环境气温低，但在某些情况下，如湿度较大、风速较小的室内或户外环境，会影响蒸发散热效率。
- 人为因素： 过度保暖的衣物是冬季热射病的关键人为风险因素。人们为了抵抗寒冷，往往选择多层或厚重的衣物，但在运动或体力劳动时，这些衣物会极大地限制汗液蒸发和对流散热。长时间停留在密闭且过度加热的车厢内，即使外部环境是冬季，也可能导致车内人员热射病死亡 18。此外，脱水也是一个重要的协同因素。在寒冷环境中，口渴感不如夏季明显，导致个体补水意识下降，而脱水会降低机体散热能力，增加热射病的风险。
因此，冬季热射病的流行病学特征强调了在寒冷季节下，对高风险场景、高危人群以及气候与人为因素的复杂相互作用进行识别和干预的重要性。
3. 冬季热射病的发病机制与风险因素
3.1 体温调节失衡的冬季特异性诱因
冬季热射病的发病机制，虽然核心仍然是产热与散热的失衡，但在低温环境下，其具体的诱发因素和生理过程呈现出独特的冬季特异性。这主要体现在散热受阻的关键机制以及运动产热的叠加效应上。
厚重衣物阻碍蒸发散热：
在冬季，人们为抵御寒冷普遍穿着多层或厚重的保暖衣物。这些衣物通常具有良好的绝热性能，可以有效减少身体向外界环境的热量传导和对流散热。然而，当个体进行剧烈运动或体力劳动时，代谢产热量急剧增加，需要通过蒸发汗液来散发大量热量以维持体温平衡。此时，厚重的衣物，特别是那些透气性差、吸湿性不佳的材质，会形成一个限制性的微环境，严重阻碍汗液从皮肤表面蒸发。汗液在衣物内部积聚，导致皮肤表面潮湿，但由于衣物饱和，实际的蒸发速率下降，从而大大降低了蒸发散热的效率2122。此外，衣物对身体的压迫也可能减少空气流通，进一步限制散热。这种“被动式”的散热障碍是冬季劳力型热射病最核心的诱因之一。室内外温差导致血管调节紊乱：
尽管冬季室外温度较低，但室内通常有暖气供应，温度较高。当人们频繁进出室内外环境时，身体的血管舒缩系统需要不断调整以适应温度变化。从温暖室内进入寒冷室外时，皮肤血管会收缩以减少热量散失；而从寒冷室外进入温暖室内，或在温暖室内进行剧烈活动时，皮肤血管会舒张以增加散热。然而，频繁或剧烈的温度变化可能导致血管调节机制的紊乱。特别是在运动产热大量增加的情况下，如果皮肤血管舒张不充分，或者在某些情况下，为了应对寒冷刺激而导致的持续性外周血管收缩，都可能影响皮肤血流量，从而抑制有效散热7。此外，长时间处于低温环境后突然进入高温环境，也可能引发体温调节的“延迟”反应，即机体未能及时开启高效散热模式。运动产热激增的叠加效应：
冬季进行的高强度运动（如滑雪、冬季长跑、高山攀登、军事训练等）本身就会导致身体代谢率显著升高，产生远超静息状态的大量热量。研究表明，在运动过程中，核心体温的升高是正常生理反应，但当产热超过散热能力时，就会导致核心体温失控性升高23。在冬季，这种运动产热的激增与上述厚重衣物造成的散热障碍、以及可能的血管调节紊乱叠加，形成了一个危险的“恶性循环”。体能消耗和疲劳也可能影响机体对冷暴露的生理反应，例如，长时间的体力消耗会削弱颤抖和血管收缩对寒冷的反应，从而影响体温维持，尽管这是指体温下降，但也提示了疲劳对体温调节的影响24。当身体为了抵御寒冷而穿着厚重衣物时，运动产生的热量无法及时散发，会在体内迅速积累，最终导致核心体温突破临界值，引发热射病。例如，在军事行动中，士兵为了应对严寒通常穿着厚重防护服，但在高强度训练或战斗中，这些服装反而会成为散热障碍，增加热射病的风险。
3.2 个体与环境协同风险因素
冬季热射病的发生并非单一因素作用的结果，而是个体内在易感性与外部环境协同作用的复杂过程。了解这些协同风险因素对于识别高危个体和制定有效的预防策略至关重要。
个体易感性因素：
- 脱水： 尽管在寒冷环境中，口渴感不如夏季强烈，但人体在冬季同样会因呼吸、出汗（尤其是在运动后）以及低湿度环境而丢失水分。脱水会减少血容量，降低皮肤血流量，从而削弱机体的有效散热能力。脱水会增加热应激的风险 25。因此，在冬季进行活动时，即便不感到口渴，也应保持规律饮水，补充足够的水分和电解质。
- 肥胖： 肥胖个体拥有更多的脂肪组织，而脂肪组织是良好的绝热体，这使得肥胖者散热更加困难。此外，肥胖通常伴随着更高的基础代谢率，从而产生更多的内源性热量。在运动时，肥胖个体需要消耗更多的能量来完成同样的运动量，导致产热量更大。这些因素共同作用，使得肥胖者在冬季进行体力活动时，更容易发生体温过高。
- 炎症状态与基础疾病： 感染、慢性炎症、甲状腺功能亢进等疾病会提高机体基础代谢率，增加产热。此外，某些慢性疾病（如心血管疾病、糖尿病、肾功能不全等）患者的体温调节系统可能受损，对热应激的耐受性较差。服用某些药物，如抗胆碱能药物、利尿剂、β受体阻滞剂、精神类药物等，也可能影响汗腺功能、血管舒缩或中枢体温调节，从而增加热射病的风险。
- 年龄因素： 婴幼儿和老年人是热射病的脆弱群体。婴幼儿的体温调节系统尚未完全发育成熟，对环境温度变化的适应能力较差。例如，有报告指出，婴儿可能因被过度包裹在床上而导致致命性热射病 26。老年人则可能因体温调节功能退化、对口渴感觉迟钝、以及常伴有多种慢性疾病和服药等因素，使其在冬季室内过度保暖或活动时面临更高的热射病风险，因此需要采取预防措施 27。
- 睡眠不足和体能不佳： 充足的睡眠对于身体的恢复和体温调节功能至关重要。睡眠不足会影响中枢神经系统对体温的调控能力。同时，体能较差或处于疲劳状态的个体，其应对热应激的能力也会下降。
环境协同因素：
- 高湿度室内环境： 湿度是影响蒸发散热效率的关键环境因素。在高湿度环境中，汗液蒸发速度减慢，导致散热效率下降，即使环境温度不高，也可能造成体热积聚。在冬季，室内通常密闭且可能存在加湿设备，如果通风不良，容易形成高湿环境，增加热射病风险 27。
- 低风速密闭空间： 风速能够加速对流散热和汗液蒸发。在通风不良的密闭空间，空气流动受限，导致皮肤表面的热量和湿气难以散发，从而阻碍散热，增加热射病发生的可能性。例如，婴儿可能因被过度包裹在床上并处于密闭环境而导致致命性热射病 26。
- 不当的穿着习惯： 过于厚重、不透气或多层叠加的衣物在冬季虽然能保暖，但如果进行剧烈活动，则会严重阻碍汗液蒸发和热量散发，将身体变成一个“保温箱”，从而显著增加热射病的风险。
这些个体和环境因素并非独立作用，而是相互交织，共同构成了冬季热射病发生的复杂风险网络。例如，一个脱水且穿着厚重衣物在通风不良的高湿度室内进行高强度运动的肥胖个体，其热射病风险将大大增加。因此，在冬季预防热射病，需要综合考虑并管理这些协同风险因素。
4. 冬季热射病的临床表现与诊断挑战
4.1 典型与非典型症状特征
冬季热射病的临床表现，与夏季热射病在核心症状上保持一致，即核心体温升高伴中枢神经系统功能障碍 28。然而，由于冬季环境的特殊性，也可能出现一些非典型症状，增加了临床诊断的复杂性，尤其是在与低温相关的疾病（如低体温症）鉴别诊断时。
典型症状特征：
- 核心体温升高： 这是热射病诊断的标志，通常指核心体温（直肠、食管或膀胱温度）升高至40°C（104°F）以上 29。体温测量应通过直肠或食道探头进行，以获取准确的核心温度，口服或腋下测温可能低估实际体温。
- 中枢神经系统功能障碍： 这是区分热射病与其他热相关疾病（如热衰竭）的关键特征 29。表现形式多样，包括意识模糊、谵妄、定向障碍、易激惹、判断力受损、言语不清、共济失调、抽搐甚至昏迷 2829。这些症状的出现提示病情严重，需要紧急干预。
- 多器官损伤表现： 热射病是一种全身性疾病，可导致多器官系统功能障碍 28。常见的表现包括：
- 心血管系统： 心动过速、血压波动（早期可能升高，后期因脱水和血管舒张过度导致低血压）、心肌损伤。
- 呼吸系统： 呼吸急促、急性呼吸窘迫综合征（ARDS）。
- 肾脏系统： 急性肾损伤，常表现为少尿、无尿，与横纹肌溶解引起的肌红蛋白尿有关。
- 肝脏系统： 肝酶升高，严重时可导致肝功能衰竭。
- 血液系统： 弥散性血管内凝血（DIC），表现为出血倾向或血栓形成。
- 肌肉系统： 广泛的横纹肌溶解，导致肌肉疼痛、肌无力，血清肌酸激酶（CK）水平显著升高。
- 胃肠道系统： 恶心、呕吐、腹泻，肠道通透性增加导致细菌内毒素进入血液，引发全身炎症反应 30。
非典型症状特征与鉴别难点：
在冬季环境下，热射病的某些表现可能被掩盖或误导，给早期识别带来挑战：
- 体表低温掩盖核心高热： 尽管核心体温显著升高，但在寒冷环境下，特别是在户外运动后，患者的皮肤可能会因环境暴露、血管收缩或降温措施（如用冷水擦拭）而触感冰凉，甚至出现鸡皮疙瘩。这种体表特征可能导致医护人员或旁观者误判为低体温症，从而延误正确的降温治疗。尤其是在穿着厚重衣物的情况下，皮肤散热受阻，体表温度可能更能反映环境温度而非核心体温，使得这一现象更为突出。
- 与低体温症的鉴别诊断： 低体温症（核心体温低于35°C）和热射病是两个截然相反的极端体温调节障碍 29。然而，在冬季运动后出现的意识障碍、肌肉僵硬、颤抖（初期可能出现，后期严重低体温则消失）、心律失常等症状，在两种疾病中都可能出现，增加了鉴别诊断的难度。准确测量核心体温是鉴别的关键。热射病患者应迅速降温，而低体温症患者则需要缓慢复温，错误的治疗方向可能带来严重后果。
- “不出汗”的误区： 在冬季，由于厚重衣物阻碍汗液蒸发，或因严重脱水，患者可能出现皮肤湿冷但汗液蒸发不畅的情况，甚至因体温调节中枢受损而停止出汗。这可能导致“不出汗就是热射病”的传统观念误导，延误对劳力型热射病患者的诊断。
因此，在冬季识别热射病，临床医生和现场急救人员需要保持高度警惕，关注患者的活动史、穿着、环境条件，并强调核心体温测量的准确性，避免被非典型体表特征所迷惑，以确保及时正确的诊断和治疗。
4.2 诊断标准与辅助工具应用
冬季热射病的诊断主要依赖于临床表现，特别是核心体温升高伴中枢神经系统功能障碍。然而，在实际操作中，准确的诊断需要标准化的测量方法和辅助工具的支持，尤其是在早期识别和鉴别诊断方面。
核心体温测量方法的必要性：
热射病的诊断标准之一是核心体温升高至40°C以上 31。因此，准确测量核心体温是诊断的基础和关键。
- 直肠温度： 直肠温度被认为是测量核心体温的金标准，因为它能较好地反映身体深部组织的温度，且受环境因素影响较小 32。在急诊和重症监护环境中，推荐使用直肠温度计进行连续监测。
- 食管温度： 食管温度也是一种可靠的核心体温测量方法，尤其适用于插管患者或在麻醉状态下进行监测 32。在运动生理学研究中，食管温度常用于精确反映核心体温的变化。
- 其他方法： 口腔温度、腋下温度、鼓膜温度和皮肤温度等方法，可能无法准确反映核心体温，因此不推荐作为热射病诊断的主要依据 31。
生物标志物在早期识别中的价值：
热射病会引起全身性炎症反应和多器官损伤，因此，监测特定的生物标志物有助于早期识别、评估疾病严重程度和判断预后 33。
- 肌酸激酶（Creatine Kinase, CK）： 运动可能导致横纹肌溶解，从而引发肌酸激酶大量释放入血 34。血清CK水平显著升高（通常可达数千至数万IU/L）是横纹肌溶解的敏感指标，可提示肌肉损伤的程度。肌红蛋白（Myoglobin）也可升高，并与急性肾损伤的发生密切相关。
- 炎症因子： 热射病诱发的全身炎症反应综合征（SIRS）是导致多器官功能障碍的重要机制 35。促炎细胞因子，如肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β) 和白细胞介素-6 (IL-6) 等水平显著升高。这些炎症因子可以作为热射病严重程度和器官损伤的潜在预测指标。
- 肝功能指标： 天冬氨酸转氨酶（AST）、丙氨酸转氨酶（ALT）和乳酸脱氢酶（LDH）等肝酶升高，可反映肝细胞损伤。
- 肾功能指标： 血肌酐（Creatinine）和尿素氮（BUN）升高是急性肾损伤的标志 33。在热射病中，急性肾损伤是常见的并发症之一。
- 凝血功能指标： 凝血酶原时间（PT）、活化部分凝血活酶时间（APTT）延长，以及血小板计数下降，提示可能存在弥散性血管内凝血（DIC）。
- 电解质紊乱： 热射病患者常伴有电解质紊乱，如高钠血症（常见于脱水）、低钠血症（可能与过度补水或抗利尿激素分泌异常有关）、高钾血症（与横纹肌溶解和肾功能不全有关）等 33。血浆中的某些肽（如血管紧张素II）的增加和另一些肽（如血管紧张素-(1-7)）的减少，可能作为肝功能障碍的潜在生物标志物 35。
鉴别诊断的重要性：
在冬季，热射病需要与低体温症、感染性休克、中枢神经系统感染、药物中毒等疾病进行鉴别。准确的核心体温测量结合详细的病史（如近期剧烈运动史、暴露史）和生物标志物检测，有助于进行正确的鉴别诊断，避免误诊误治。例如，婴儿死于热射病的案例中，对热射病早期识别和恰当处理至关重要 36。对于糖尿病肾病患者，发烧、低血压和横纹肌溶解症也需要与热射病进行鉴别。
通过综合运用核心体温测量方法和对关键生物标志物的监测，可以提高热射病的早期识别率和诊断准确性，为及时有效的治疗争取宝贵时间。及时有效的治疗对热射病患者的预后至关重要 37。
5. 冬季热射病的急救与治疗策略优化
5.1 现场急救的冬季适配性调整
热射病的现场急救目标是迅速降低核心体温，以限制高温对机体造成的损害，并改善患者预后。在冬季，尽管环境温度较低，但热射病患者的现场急救策略需要进行适配性调整，以平衡快速降温的有效性与避免医源性低体温的风险。
对比夏季降温方法：
夏季热射病的现场降温常采用“浸泡-蒸发-传导”联合的方式，其中冷水浸泡被认为是降温速度最快、效果最好的方法之一 383940。在水温1-17°C的冷水或冰水浸泡下，可显著降低核心体温 3839。蒸发冷却（如喷洒温水并用风扇吹拂）也因其操作简便、对设备要求低而在现场广泛应用。
然而，在冬季进行现场急救时，直接照搬夏季的降温策略可能面临以下挑战和风险：
冷水浸泡的可行性与风险：
- 可行性限制： 在冬季的户外场景（如滑雪场、冬季训练场地），迅速找到足够量的冰水或冷水进行全身浸泡可能存在实际困难。此外，将患者完全浸入冰水或冷水中，需要克服患者的寒冷应激反应，以及医护人员在低温环境下操作的挑战。
- 避免低体温的风险： 虽然快速降温是热射病急救的关键，但在冬季较低的环境温度下，过度或长时间的强效降温可能导致患者核心体温过低，诱发医源性低体温症。低体温症本身可能导致心律失常、凝血功能障碍和免疫功能抑制等严重并发症。因此，在实施冷水浸泡时，必须密切监测核心体温，一旦达到目标温度（通常建议降至38-39°C），应立即停止降温，并采取措施保持体温稳定，避免过冷。
蒸发冷却的效率与局限性：
- 效率降低： 蒸发冷却依赖于环境空气的流动和湿度。在冬季的户外，风速可能较大，有利于蒸发；但若在室内或避风处，空气湿度可能较高，影响汗液或喷洒水分的蒸发效率。同时，冬季人们常穿着厚重衣物，这会阻碍皮肤表面水分的蒸发。
- 操作难度： 移除厚重衣物以暴露皮肤，并在寒冷环境中喷洒温水或冷水并用风扇吹拂，可能会使患者感到极度不适，并可能增加低体温的风险。
现场冷源选择与操作规范：
鉴于冬季环境的特殊性，现场急救应优先选择快速有效且可控的降温方法，并密切关注患者体温变化，防止过冷。
优先推荐：冰敷/冷敷关键区域：
- 部位选择： 将冰袋或冷敷物放置在腹股沟、腋窝、颈部等大血管走行区域，这些部位能够高效传导热量，迅速降低核心体温。
- 操作： 使用冰袋、冷湿毛巾或冬季易得的冷水瓶等，持续对这些区域进行冷敷。可与移除部分厚重衣物、增加通风结合。
- 优势： 这种方法相对容易实施，所需冷源量较少，且能够实现较快的降温速度，同时降低了全身浸泡可能带来的低体温风险。
蒸发冷却的冬季适配：
- 室内应用： 若在室内环境，可移除患者厚重衣物，用温水或冷水擦拭皮肤，并使用风扇吹拂，同时确保室内有足够的通风。
- 户外谨慎： 在户外，若环境风速较低，可考虑移除部分厚重衣物后进行擦拭降温。但需警惕寒冷环境中的风寒效应，避免患者体温骤降。
其他降温辅助措施：
- 静脉输注冷生理盐水： 在专业医护人员在场时，可考虑静脉快速输注4°C的生理盐水，以辅助内部降温。
- 环境控制： 将患者转移到阴凉、通风良好的地方，避免阳光直射或密闭高温环境。
操作规范强调：
- 持续监测核心体温： 使用直肠温度计进行持续监测是至关重要的。降温目标通常是快速将核心体温降至38-39°C，一旦达到目标，应立即停止积极降温，并注意保温，防止体温持续下降。
- 早期识别与快速启动： 热射病降温的“黄金时间”非常短，发病后30分钟内开始降温可显著改善预后。因此，现场人员应受过专业训练，能迅速识别并启动急救措施。
- 兼顾低体温预防： 在降温过程中，医护人员需密切观察患者是否出现低体温的早期迹象（如寒战、皮肤湿冷、心律减慢等），并随时准备采取保暖措施。
- 紧急医疗系统启动： 无论采取何种现场降温措施，都应同时启动紧急医疗服务，将患者尽快转运至具备高级生命支持和多器官功能监测能力的医疗机构。
通过以上调整和规范，可以在冬季环境下更安全、有效地对热射病患者实施现场急救，从而最大程度地降低并发症和死亡风险。
5.2 院内多器官支持与并发症管理
热射病是一种多系统疾病，可迅速导致多器官功能障碍综合征（MODS），甚至死亡 41424344。因此，在患者被转运至医院后，除了持续降温以尽快将核心体温恢复正常范围外，全面的多器官支持和并发症管理是治疗成功的关键。
1. 循环功能支持：
热射病患者常出现循环不稳定，表现为心动过速、低血压，严重时可发展为休克。
- 液体复苏： 初期应积极进行静脉液体复苏，以纠正脱水和改善循环血容量。然而，需注意避免过度输液，以免加重心脏负荷或导致肺水肿。补液种类通常选择等渗晶体液。
- 血管活性药物： 若液体复苏后低血压仍无法纠正，可考虑使用血管活性药物（如去甲肾上腺素、多巴胺）维持平均动脉压，确保重要器官的灌注。
- 心功能监测： 对心功能进行密切监测，包括心电图、心脏超声，以早期发现心肌损伤或心律失常，并及时进行干预。热射病可能引起心血管功能障碍，包括心肌细胞损伤和心律失常。
2. 肾脏功能支持：
急性肾损伤是热射病常见的严重并发症，主要与横纹肌溶解导致的肌红蛋白尿、低血容量和直接热损伤有关 42。
- 水合与利尿： 积极的液体复苏有助于维持肾脏灌注，减少肌红蛋白在肾小管的沉积。必要时可使用利尿剂，维持足够的尿量，促进毒素排出。
- 碱化尿液： 肌红蛋白在酸性环境中易形成沉淀，加重肾小管损伤。因此，通过静脉滴注碳酸氢钠碱化尿液，有助于减少肌红蛋白肾毒性。
- 肾脏替代治疗： 若出现严重的急性肾损伤，表现为无尿、严重电解质紊乱（如高钾血症）或酸中毒，应及时启动血液透析或连续性肾脏替代治疗（CRRT）。
3. 神经功能支持：
- 颅内压监测与管理： 严重的热射病可能引起脑水肿，导致颅内压升高。对存在持续性昏迷或神经系统恶化的患者，应考虑进行颅内压监测，并采取相应措施（如甘露醇、限制液体、维持头部抬高）降低颅内压。
- 抗惊厥治疗： 若出现抽搐，应立即给予苯二氮卓类药物等抗惊厥治疗。
- 镇静与肌松： 对于烦躁不安或持续抽搐的患者，可能需要镇静甚至肌松治疗，以减少代谢产热，保护神经功能。
- 血糖管理： 密切监测血糖，避免高血糖或低血糖对神经系统的损害。
4. 炎症反应调控与并发症管理：
热射病不仅是高温损伤，更是一种全身性炎症反应综合征。过度炎症反应是导致多器官功能障碍的关键机制之一 4345。
- 糖皮质激素（如地塞米松）的应用： 糖皮质激素具有强大的抗炎和免疫抑制作用。研究表明，地塞米松可以改善热射病引起的超凝状态、促炎细胞因子过量产生、动脉低血压以及脑缺血和器官损伤 46。它通过抑制炎症因子（如TNF-α、IL-1β）的释放和改善凝血功能，从而减轻多器官损伤。然而，其应用的时机、剂量以及对预后的长期影响仍需进一步研究，并非所有患者均常规使用。
- 其他并发症管理：
- 横纹肌溶解： 除了上述肾功能支持外，还需监测血清肌酸激酶（CK）和肌红蛋白水平，并警惕高钾血症的发生。
- 凝血功能障碍： 热射病可导致弥散性血管内凝血（DIC），表现为出血或血栓形成。需密切监测凝血指标，必要时给予血制品（如新鲜冰冻血浆、血小板）纠正凝血功能障碍。
- 感染控制： 热射病患者免疫功能受损，易发生感染。应加强感染监测，必要时给予经验性抗生素治疗。
- 电解质紊乱： 纠正各种电解质紊乱，如高钾、低钠等。
在冬季热射病的院内管理中，强调持续、准确的核心体温监测，并根据患者具体情况，个体化地制定多器官支持和并发症管理方案，以最大程度地提高患者的生存率和改善预后。
6. 冬季热射病的预防体系构建
6.1 个体层面的主动防护
在冬季，个体层面的主动防护是预防热射病的关键，尤其对于参与冬季运动或户外活动的人群。有效的预防措施需要综合考虑运动前的准备、运动中的管理以及对环境变化的适应。
运动前热适应训练：
尽管在寒冷环境中进行热适应训练听起来有些矛盾，但其核心在于增强身体应对热应激的能力。在冬季户外运动季开始前或在高强度训练前，可以通过以下方式进行：衣物分层管理：
衣物选择是冬季运动中影响体温调节最重要的因素之一。- 三层着装原则：
- 内层（排汗层）： 贴身穿着吸湿排汗的材料，如聚酯纤维或美利奴羊毛，能迅速将汗水从皮肤表面导出，保持皮肤干爽。避免纯棉衣物，因为棉吸水后不易干燥，会带走体热，同时阻碍蒸发散热。
- 中层（保暖层）： 选择抓绒、羽绒或合成材料填充的衣物，提供主要保暖功能。根据运动强度和环境温度，可穿脱此层以调节体温。
- 外层（防护层）： 具有防风、防水、透气功能的冲锋衣或软壳衣。用于阻挡风雪，同时允许身体内部产生的湿气排出。
- 动态调整： 在运动过程中，应根据身体感受和运动强度，及时增减衣物。在开始运动前可能感到稍冷是正常的，因为运动很快会产生大量热量。停止运动休息时，应立即添加保暖衣物，防止体温过快下降。
- 头部、手部和足部防护： 这些部位是热量散失的重要途径，应佩戴帽子、手套和厚袜子，但同样需注意透气性，避免局部过热。
- 三层着装原则：
补水与电解质监测：
冬季运动中的脱水风险常被低估，但其对热射病的易感性影响巨大 49。冬季运动强度与环境的动态调整：
- 倾听身体信号： 密切关注身体发出的过热信号，如过度出汗、疲劳加剧、头晕、恶心、肌肉痉挛等，一旦出现应立即停止活动并寻求帮助。
- 计划休息： 定期安排休息时间，尤其是在长时间运动中，以便身体散热和补充水分。休息时应选择避风、相对温暖的区域。
- 避免高峰时段： 避免在一天中最冷或风速最大的时段进行高强度户外运动。
- 适应环境： 如果环境湿度高或通风不良，应适当降低运动强度或缩短运动时间。对于在室内过度供暖环境中运动，更应加强通风，或选择气温适宜的室内环境。
- 团队互助： 集体活动中应相互观察，及时发现队友可能出现的过热迹象。
通过上述个体层面的主动防护措施，可以显著降低冬季热射病的发生风险，确保冬季运动和户外活动的安全进行。
6.2 组织与公共卫生层面的协同干预
冬季热射病的预防不仅仅是个体行为，还需要组织和公共卫生层面的协同干预，以构建一个更全面的防护体系，尤其针对冬季运动组织方、户外作业单位以及特定脆弱人群。
冬季运动/作业的环境风险评估与管理：
- 温湿度监测： 组织方应建立常态化的环境温湿度监测机制。对于室内场馆，应确保合理的温度和湿度控制，避免过度加热和高湿环境，并保障良好的通风条件。例如，应定期监测空气质量，包括挥发性有机化合物（VOCs）浓度，以确保室内环境安全 5253。户外运动则需关注日间气温、风速等气象指标。
- 通风状况评估： 尤其是在密闭或半密闭空间（如大型体育馆、冬季帐篷休息区），应评估和改善通风系统，确保空气流通，促进热量和湿气散发。
- 运动强度限制与调整： 依据环境风险评估结果，制定相应的运动强度指南或作业规范。例如，当室内环境过热或通风不良时，应建议降低运动强度、缩短运动时间或增加休息频率。在极寒天气下，为防止穿戴过度保暖而导致的内部过热，也应适当调整户外运动或作业的时长与强度。
- 场地材料考量： 对于冬季运动场地，特别是人造草坪等合成材料场地的选择，需考量其对环境微气候的影响以及潜在的健康风险，例如，合成草坪中的多环芳烃（PAHs）在降雨事件中释放，可能对人体健康构成潜在致癌风险 5455。虽然这主要涉及污染物暴露，但也提示了场地环境因素的复杂性。
应急预案的建立与实施：
- 冷源储备与快速获取： 鉴于冬季热射病现场急救的特殊性，组织方应提前储备充足的冷源，如大量冰块、冰袋、冷水浴缸或可快速充气的冷水池。这些冷源应放置在运动/作业区域附近，确保在紧急情况下能在最短时间内获取并使用。冷水浸泡被认为是降温速度最快、最有效的现场急救方法 3840。
- 快速转运机制： 建立高效的医疗转运流程和快速响应机制。一旦发生热射病，应立即启动急救程序，并在实施初步降温的同时，迅速将患者转运至具备高级生命支持能力的医疗机构。转运过程中应持续进行降温处理，遵循“先降温，后转运”的原则，因为早期和快速降温是改善热射病预后的关键 5657。
- 急救人员培训： 对所有相关的教练、领队、赛事组织者、安保人员及户外作业负责人进行热射病识别、现场急救（包括准确的核心体温测量方法）及转运流程的专业培训。强调在冬季环境下，如何平衡快速降温与避免医源性低体温的风险。
特殊人群的健康宣教体系：
- 老年人与慢性病患者： 针对老年人、心血管疾病、糖尿病患者等特殊人群，公共卫生机构应开展有针对性的健康宣教。重点宣传在冬季室内过度取暖的潜在风险，以及如何在保暖的同时确保有效散热（如穿着轻便透气的居家服、保持室内适当通风、避免在高温室内进行剧烈活动等）。此外，强调规律补水的重要性，即使在不感到口渴时也要适量饮水。需要注意的是，极端温度对心血管疾病发病率的影响在寒冷天气中更为显著 58。
- 儿童和青少年： 针对儿童和青少年，特别是参与冬季体育活动的群体，宣教内容应包括：合理着装、运动中及时补充水分、关注身体不适信号、以及避免在密闭或过度加热的环境中长时间剧烈运动。应强调身体活动作为暴露因素对健康风险评估的重要性，并制定在不同环境污染水平下的儿童青少年活动指南 59。
- 普及热射病知识： 通过多种渠道（社区讲座、媒体宣传、宣传册、手机应用等）向公众普及冬季热射病的基本知识，包括其概念、风险因素、早期症状识别和正确的急救措施。特别要纠正“冬季不会发生热射病”的错误观念，提升公众对冬季热射病的警惕性。
通过组织和公共卫生层面的协同努力，建立健全的风险评估、应急响应和健康宣教体系，将显著提升冬季热射病的预防和管理水平，从而有效保护公众健康。
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参考文献
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Recently, the incidence of heat-related illnesses has exhibited a steadily upward trend, which is closely associated with several environmental factors such as climate change and air pollution. The progression of heat-related illnesses is a continuous process and can progress to the terminal period when it transforms into heat stroke, the most severe form. Heat stroke is markedly by a core body temperature above 40°C and central nervous system dysfunction. Current knowledge suggests that the pathogenesis of heat stroke is complex and varied, including inflammatory response, oxidative stress, cell death, and coagulation dysfunction. This review consolidated recent research progress on the pathophysiology and pathogenesis of heat stroke, with a focus on the related molecular mechanisms. In addition, we reviewed common strategies and sorted out the drugs in various preclinical stages for heat stroke, aiming to offer a comprehensive research roadmap for more in-depth researches into the mechanisms of heat stroke and the reduction in the mortality of heat stroke in the future.
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Abderrezak Bouchama, Bisher Abuyassin, Cynthia Lehe, et al.
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In the past two decades, record-breaking heatwaves have caused an increasing number of heat-related deaths, including heatstroke, globally. Heatstroke is a heat illness characterized by the rapid rise of core body temperature above 40 °C and central nervous system dysfunction. It is categorized as classic when it results from passive exposure to extreme environmental heat and as exertional when it develops during strenuous exercise. Classic heatstroke occurs in epidemic form and contributes to 9-37% of heat-related fatalities during heatwaves. Exertional heatstroke sporadically affects predominantly young and healthy individuals. Under intensive care, mortality reaches 26.5% and 63.2% in exertional and classic heatstroke, respectively. Pathological studies disclose endothelial cell injury, inflammation, widespread thrombosis and bleeding in most organs. Survivors of heatstroke may experience long-term neurological and cardiovascular complications with a persistent risk of death. No specific therapy other than rapid cooling is available. Physiological and morphological factors contribute to the susceptibility to heatstroke. Future research should identify genetic factors that further describe individual heat illness risk and form the basis of precision-based public health response. Prioritizing research towards fundamental mechanism and diagnostic biomarker discovery is crucial for the design of specific management approaches.
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Heatstroke is a syndrome consisting of life-threatening central nervous system and multiple organ dysfunction from complications of hyperthermia. Additionally, there is an associated complex immunological and inflammatory component to the illness that resembles sepsis. Core body temperature exceeds 40 degrees C with associated mental status changes such as delirium and coma. Generalized tonic/clonic seizures can occur. A variable degree of organ involvement is present that contributes to the severity of the medical picture. Heatstroke can be viewed as a tropical neurological disorder especially for unacclimated travelers going to warm climates. Heatstroke can be categorized into two types depending on the cause. Classic heatstroke is nonexertional, environmentally related and exertional heatstroke occurs in the setting of strenuous exercise. Heatstroke is actually the most severe of a continuum of heat-related illnesses that carries a high incidence of mortality. Treatment is directed at rapidly reducing core body temperature and the management of life-threatening systemic complications.
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Heatstroke is a life-threatening and the most severe form of heat-related illnesses, characterized by body temperature >40ºC and central nervous system dysfunction. Heatstroke is classified into Non-Exertional Heatstroke (NEHS) and Exertional Heatstroke (EHS). The pathophysiology of heatstroke involves a combination of direct heat effects on the host, the systemic inflammatory and coagulopathic response. The diagnosis of heatstroke based on Bouchama's definition or Japan Association of Acute Medicine (JAAM) criteria. The basic principle of heatstroke management is early resuscitation and immediate cooling. Cold water immersion or convection evaporation method can be implemented based on the specific patient characteristic. Preventive strategies are early recognition by health workers, socialization to vulnerable groups and adequate acclimatization.
5Heat StrokePubMed
Andrew Morris, Gaurav Patel
Heat-related illness is a spectrum of conditions progressing from heat exhaustion and heat injury to life-threatening heat stroke. Heat stroke is a clinical constellation of symptoms that include a severe elevation in body temperature, typically, but not always, greater than 40°C. Also, there must be clinical signs of central nervous system dysfunction, including ataxia, delirium, or seizures, in the setting of exposure to hot weather or strenuous physical exertion. Risk factors include environmental variables, medications, drug use, and other medical comorbidities.
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Michael Horseman, Ladan Panahi, George Udeani, et al.
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Humans maintain core body temperature via a complicated system of physiologic mechanisms that counteract heat/cold fluctuations from metabolism, exertion, and the environment. Overextension of these mechanisms or disruption of body temperature homeostasis leads to bodily dysfunction, culminating in a syndrome analogous to exertional heat stroke (EHS). The inability of this thermoregulatory process to maintain the body temperature is caused by either thermal stress or certain drugs. EHS is a syndrome characterized by hyperthermia and the activation of systemic inflammation. Several drug-induced hyperthermic syndromes may resemble EHS and share common mechanisms. The purpose of this article is to review the current literature and compare exertional heat stroke (EHS) to three of the most widely studied drug-induced hyperthermic syndromes: malignant hyperthermia (MH), neuroleptic malignant syndrome (NMS), and serotonin syndrome (SS). Drugs and drug classes that have been implicated in these conditions include amphetamines, diuretics, cocaine, antipsychotics, metoclopramide, selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and many more. Observations suggest that severe or fulminant cases of drug-induced hyperthermia may evolve into an inflammatory syndrome best described as heat stroke. Their underlying mechanisms, symptoms, and treatment approaches will be reviewed to assist in accurate diagnosis, which will impact the management of potentially life-threatening complications.
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Miles Marchand, Kenneth Gin
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Masahide Kondo, Masaji Ono, Kouichi Nakazawa, et al.
Environ Health Prev Med. 2013 May;18(3):251-7. doi: 10.1007/s12199-012-0313-7. Epub 2012 Nov 17.
OBJECTIVES: Heatstroke due to a heat wave during the summer is one of the commonly known health impacts of climate change in Japan. The elderly are particularly at high-risk of developing indoor heatstroke with poor prognosis. This study aims to describe the population among elderlies at high-risk of indoor heatstroke by focusing on the usage of cooling appliances. METHODS: We conducted a web-based household survey in eight urban areas during the winter season of 2011. Households with a person aged 65 and over were selected as samples from panel members of a research firm, and the oldest member of the household was queried about his/her usage of cooling appliances. The population at high-risk of indoor heatstroke is defined as the elderly staying in a room without cooling appliances, or not using the installed cooling appliances, or turning the cooling appliances on only when the room temperature is above 28 °C. RESULTS: 15.4 and 19.1 % of the elderlies living in urban areas of Japan are identified as at high-risk of indoor heatstroke during activity time and sleeping time, respectively, according to the definition of high-risk of indoor heatstroke in this study. CONCLUSIONS: These figures are not negligible since the consequences of heatstroke are grave, but its risk can be eliminated by an appropriate usage of cooling appliances. The preventive interventions are needed to protect the elderlies at high-risk of heatstroke.
11Heat-Related Illnesses.PubMed
Robert Gauer, Bryce K Meyers
Am Fam Physician. 2019 Apr 15;99(8):482-489.
Heat-related illnesses comprise a spectrum of syndromes resulting from disruption of thermoregulation in people exposed to high environmental heat. Symptoms range from heat edema and exercise-associated muscle cramps to exercise-associated collapse, heat exhaustion, and life-threatening heat stroke. Athletes, outdoor laborers, and military personnel are at greatest risk. Several intrinsic and extrinsic factors increase the risk of heat-related illness, including medical conditions, environmental factors, medication use, and inadequate acclimatization. Proper recognition and treatment are effective in preventing adverse outcomes. Management of the mildest forms of heat-related illness (e.g., heat edema, exercise-associated muscle cramps) is largely supportive, and sequelae are rare. Heat exhaustion is characterized by cardiovascular hypoperfusion and a rectal core temperature up to 104°F without central nervous dysfunction. Mild cooling, rest, and hydration are recommended. Heat stroke is a medical emergency in which patients present with rectal core temperature of 105°F or greater, multiorgan damage, and central nervous dysfunction. Ice water or cold water immersion is recommended. Patients adequately cooled within 30 minutes have excellent outcomes. Patients with heat stroke generally require hospitalization to monitor for medical complications despite rapid cooling. People diagnosed with heat stroke or severe heat-related illness should refrain from physical activity for at least seven days after release from medical care, then gradually begin activity over two to four weeks. Acclimatization, adequate hydration, and avoidance of activities during extreme heat are the most effective measures to reduce the incidence of heat-related illnesses.
12International Olympic Committee consensus statement on thermoregulatory and altitude challenges for high-level athletes.PubMed
M F Bergeron, R Bahr, P Bärtsch, et al.
Br J Sports Med. 2012 Sep;46(11):770-9. doi: 10.1136/bjsports-2012-091296. Epub 2012 Jun 9.
Challenging environmental conditions, including heat and humidity, cold, and altitude, pose particular risks to the health of Olympic and other high-level athletes. As a further commitment to athlete safety, the International Olympic Committee (IOC) Medical Commission convened a panel of experts to review the scientific evidence base, reach consensus, and underscore practical safety guidelines and new research priorities regarding the unique environmental challenges Olympic and other international-level athletes face. For non-aquatic events, external thermal load is dependent on ambient temperature, humidity, wind speed and solar radiation, while clothing and protective gear can measurably increase thermal strain and prompt premature fatigue. In swimmers, body heat loss is the direct result of convection at a rate that is proportional to the effective water velocity around the swimmer and the temperature difference between the skin and the water. Other cold exposure and conditions, such as during Alpine skiing, biathlon and other sliding sports, facilitate body heat transfer to the environment, potentially leading to hypothermia and/or frostbite; although metabolic heat production during these activities usually increases well above the rate of body heat loss, and protective clothing and limited exposure time in certain events reduces these clinical risks as well. Most athletic events are held at altitudes that pose little to no health risks; and training exposures are typically brief and well-tolerated. While these and other environment-related threats to performance and safety can be lessened or averted by implementing a variety of individual and event preventative measures, more research and evidence-based guidelines and recommendations are needed. In the mean time, the IOC Medical Commission and International Sport Federations have implemented new guidelines and taken additional steps to mitigate risk even further.
13Cardiovascular Effects of Compression Garments During Uncompensable Heat Stress.PubMed
Joshua Bautz, David Hostler, Priya Khorana, et al.
J Strength Cond Res. 2021 Apr 1;35(4):1058-1065. doi: 10.1519/JSC.0000000000002852.
Bautz, J, Hostler, D, Khorana, P, and Suyama, J. Cardiovascular effects of compression garments during uncompensable heat stress. J Strength Cond Res 35(4): 1058-1065, 2021-This study examined the potential hemodynamic benefits of wearing lower extremity compression garments (CGs) beneath thermal protective clothing (TPC) worn by wildland firefighters, while exercising in a heated environment. Using in a counterbalanced design, 10 male subjects ([mean ± SD] age 27 ± 6 years, height 1.78 ± 0.09 m, body mass 74.8 ± 7.0 kg, body fat 10.6 ± 4.2%, and V̇o2max 57.8 ± 9.3 ml·kg-1·min-1) completed control (no CG) and experimental (CG) conditions in randomly assigned order. Protocols were separated by a minimum of 3 days. Subjects exercised for 90 minutes (three, 30-minute segments) on a treadmill while wearing wilderness firefighter TPC and helmet in a heated room. Venous blood was drawn before and after exercise to measure hemoglobin (Hgb), hematocrit (Hct), serum osmolarity (OSM), and serum creatine phosphokinase (CPK). Vital signs and perceptual measures of exertion and thermal comfort were recorded during the protocol. Data were analyzed by the paired t-test. There were no differences in the change in heart rate (84 ± 27 vs. 85 ± 14 b·min-1, p = 0.9), core temperature rise (1.8 ± 0.6 vs. 1.9 ± 0.5° C, p = 0.39), or body mass lost (-1.72 ± 0.78 vs. -1.77 ± 0.58 kg, p = 0.7) between the conditions. There were no differences in the change in Hgb (0.49 ± 0.66 vs. 0.33 ± 1.11 g·dl-1, p = 0.7), Hct (1.22 ± 1.92 vs. 1.11 ± 3.62%, p = 0.9), OSM (1.67 ± 6.34 vs. 6.22 ± 11.39 mOsm·kg-1, p = 0.3), or CPK (22.2 ± 30.2 vs. 29.8 ± 19.4 IU·L-1, p = 0.5). Total distance walked (3.9 ± 0.5 vs. 4.0 ± 0.5 miles, p = 0.2), exercise interval (88.6 ± 3.5 vs. 88.4 ± 3.6 minutes, p = 0.8), and perceptual measures were similar between conditions. Compression garments worn beneath TPC did not acutely alter the physiologic response to exertion in TPC. With greater use in the general public related to endurance activities, the data neither encourage nor discourage CG use during uncompensable heat stress.
14Comparison of active cooling devices with passive cooling for rehabilitation of firefighters performing exercise in thermal protective clothing: a report from the Fireground Rehab Evaluation (FIRE) trial.PubMed
David Hostler, Steven E Reis, James C Bednez, et al.
Prehosp Emerg Care. 2010 Jul-Sep;14(3):300-9. doi: 10.3109/10903121003770654.
BACKGROUND: Thermal protective clothing (TPC) worn by firefighters provides considerable protection from the external environment during structural fire suppression. However, TPC is associated with physiologic derangements that may have adverse cardiovascular consequences. These derangements should be treated during on-scene rehabilitation periods. OBJECTIVE: To examine heart rate and core temperature responses during the application of four active cooling devices, currently being marketed to the fire service for on-scene rehabilitation, and compare them with passive cooling in a moderate temperature (approximately 24 degrees C) and with an infusion of cold (4 degrees C) saline. METHODS: Subjects exercised while they were wearing TPC in a heated room. Following an initial exercise period (bout 1), the subjects exited the room, removed the TPC, and for 20 minutes cooled passively at room temperature, received an infusion of cold normal saline, or were cooled by one of four devices (fan, forearm immersion in water, hand cooling, or water-perfused cooling vest). After cooling, the subjects donned the TPC and entered the heated room for another 50-minute exercise period (bout 2). RESULTS: The subjects were not able to fully recover core temperature during a 20-minute rehabilitation period when provided rehydration and the opportunity to completely remove the TPC. Exercise durations were shorter during bout 2 when compared with bout 1 but did not differ by cooling intervention. The overall magnitudes and rates of cooling and heart rate recovery did not differ by intervention. CONCLUSIONS: No clear advantage was identified when active cooling devices and cold intravenous saline were compared with passive cooling in a moderate temperature after treadmill exercise in TPC.
15Heat- and cold-induced injuries in athletes: evaluation and management.PubMed
Benjamin Noonan, Richard W Bancroft, Joshua S Dines, et al.
J Am Acad Orthop Surg. 2012 Dec;20(12):744-54. doi: 10.5435/JAAOS-20-12-744.
Both extreme heat and cold can be challenging for athletes during training and competition. One role of the team physician is to educate coaches and athletes on the risks of exposure to these conditions and how to best prevent and manage their adverse effects. Heat illness varies in degree from mild to severe, with the most severe forms being potentially fatal. Cold exposure can result in systemic effects and peripheral injury to the extremities.
16Aldosterone and vasopressin responses in the heat: hydration level and exercise intensity effects.PubMed
S J Montain, J E Laird, W A Latzka, et al.
Med Sci Sports Exerc. 1997 May;29(5):661-8. doi: 10.1097/00005768-199705000-00012.
We examined the separate and combined effects of hypohydration level and exercise intensity on aldosterone (ALD) and arginine vasopressin (AVP) responses during exercise-heat stress. Nine heat acclimated men performed 50 min of treadmill exercise in a warm room (30 degrees C dry bulb (DB), 50% relative humidity (RH) at 25%, 45% and 65% VO2max when euhydrated and when hypohydrated by 3% and 5% of body weight. Blood samples were drawn at rest and at 20 min of exercise. ALD and AVP increased (P < 0.05) in a graded manner with hypohydration level, and this effect persisted during exercise-heat stress. High intensity exercise produced greater ALD and AVP increases than low intensity exercise. ALD responses during exercise were independent of hypohydration level. AVP responses were closely related to osmolality (N = 6 of 7 subjects; r = 0.51 to r = 0.98; average r = 0.84) despite varying hydration, exercise intensity, or core temperature. We conclude that: 1) ALD and AVP increase in a graded manner with hypohydration, and this effect persists during exercise-heat stress; 2) ALD and AVP increases elicited by exercise are greater during high intensity than low intensity exercise; 3) Hypohydration and exercise intensity have additive effects on ALD: and 4) AVP responses are closely coupled to osmolality.
17Heat stroke deaths caused by electric blankets: case report and review of the literature.PubMed
Yiwu Zhou, Ling Li, Liang Liu, et al.
Am J Forensic Med Pathol. 2006 Dec;27(4):324-7. doi: 10.1097/01.paf.0000233567.51784.31.
Heat stroke is the most serious and potentially life-threatening condition of the heat-related illnesses. Heat stroke deaths caused by electric blanket are rarely reported. In this paper, we report 2 cases of fatal heat stroke caused by overheating from electric blankets in winter. One was a 41-year-old man who was found unresponsive in bed on an electric blanket. His wife shared the same bed with him and was found unconscious. The wife's axillary temperature was 40 degrees C (104 degrees C) when she was admitted to the hospital. She fully recovered after medical treatment. The husband was pronounced dead at scene, with rectal temperature at 41.2 degrees C (106.2 degrees C). The other was a 13-year-old girl who was found dead in bed on an electric blanket, with rectal temperature at 41 degrees C (105.8 degrees F). The literature is reviewed, and the pertinent findings, including scene investigations, postmortem examination, the risk and mechanism of fatal heat stroke caused by using electric blanket, are discussed.
18Death as a result of heat stroke in a vehicle: an adult case in winter confirmed with reconstruction and animal experiments.PubMed
P M Ng'walali, K Kibayashi, K Yonemitsu, et al.
J Clin Forensic Med. 1998 Dec;5(4):183-6. doi: 10.1016/s1353-1131(98)90131-6.
A 54-year-old man was found dead in the driver's seat of his vehicle on a winter's day. Investigations of the vehicle revealed that the engine was running, and the car heater was left on with the maximum temperature and velocity. The body was found excessively sweating. Rectal temperature of the body was 43 degrees C at 10 h post mortem. In autopsy, several superficial skin burns were observed on the face, the shoulders and the legs. The lungs were heavily congested and hemorrhagic. The liver showed typical alcohol-induced micronodular cirrhosis. The alcohol concentrations were 0.17% in the blood of both the left and the right heart, 0.17% in the femoral-vein blood, 0.21% in the bladder urine and 0.34% in the gastric contents. A reconstruction experiment demonstrated that the temperature inside the vehicle rose rapidly and reached 50-58 degrees C in 3 h. Animal experiments showed that the temperature threshold for rats to succumb to heat was between 40 and 45 degrees C. This case shows that heat stroke in a vehicle can occur in adults with chronic diseases or alcoholism, such as in this particular case, even in the winter.
19Evaluating infant core temperature response in a hot car using a heat balance model.PubMed
Andrew J Grundstein, Sarah V Duzinski, David Dolinak, et al.
Forensic Sci Med Pathol. 2015 Mar;11(1):13-9. doi: 10.1007/s12024-014-9619-7. Epub 2014 Oct 21.
PURPOSE: Using a 1-year old male infant as the model subject, the objectives of this study were to measure increased body temperature of an infant inside an enclosed vehicle during the work day (8:00 am-4:00 pm) during four seasons and model the time to un-compensable heating, heat stroke [>40 °C (>104 °F)], and critical thermal maximum [>42 °C (>107.6 °F)]. METHODS: A human heat balance model was used to simulate a child's physiological response to extreme heat exposure within an enclosed vehicle. Environmental variables were obtained from the nearest National Weather Service automated surface observing weather station and from an observational vehicular temperature study conducted in Austin, Texas in 2012. RESULTS: In all four seasons, despite differences in starting temperature and solar radiation, the model infant reached heat stroke and demise before 2:00 pm. Time to heat stroke and demise occurred most rapidly in summer, at intermediate durations in fall and spring, and most slowly in the winter. In August, the model infant reached un-compensable heat within 20 min, heat stroke within 105 min, and demise within 125 min. The average rate of heating from un-compensable heat to heat stroke was 1.7 °C/h (3.0 °F/h) and from heat stroke to demise was 4.8 °C/h (8.5 °F/h). CONCLUSIONS: Infants left in vehicles during the workday can reach hazardous thermal thresholds quickly even with mild environmental temperatures. These results provide a seasonal analogue of infant heat stroke time course. Further effort is required to create a universally available forensic tool to predict vehicular hyperthermia time course to demise.
20[Environmental risk factors in the territory of military operations in Iraq and Afghanistan].PubMed
Krzysztof Korzeniewski
Pol Merkur Lekarski. 2008 Jul;25(145):5-8.
Military service in Iraq and Afghanistan is burdened by series of environmental factors such as high and low air temperature, wind, sand, dust, and local fauna. In summertime the main hazard are heat injuries. Sand and dust storms also become troublesome. In the winter another health problem is effect of low temperature. In Afghanistan additional threat pose mountain conditions, especially in wintertime when appear intense snowfalls. Hard conditions more than once characteristic for duty of Stabilization Forces soldiers in both countries can cause significant threat for health and life.
21Protective clothing and heat stress.PubMed
I Holmér
Ergonomics. 1995 Jan;38(1):166-82. doi: 10.1080/00140139508925093.
The high level of protection required by protective clothing (PPC) severely impedes heat exchange by sweat evaporation. As a result work associated with wearing PPC, particularly in hot environments, implies considerable physiological strain and may render workers exhausted in a short time. Current methods of describing evaporative heat exchange with PPC are insufficient, will overestimate evaporative heat loss and should not be recommended. More reliable measures of the resistance to evaporative heat transfer by PPC should be developed and standardized. Direct measurements of evaporative resistance of PPC may be carried. However, a more promising method appears to be the definition of evaporative resistance on the basis of the icl-index for the fabric layers. The icl-index is a permeation efficiency ratio, which in combination with clothing insulation determines the evaporative heat transfer. Current methods should be further developed to account for effects of moisture condensation and microclimate ventilation.
22Physiological interactions with personal-protective clothing, physically demanding work and global warming: An Asia-Pacific perspective.PubMed
Nigel A S Taylor, Joo-Young Lee, Siyeon Kim, et al.
J Therm Biol. 2021 Apr;97:102858. doi: 10.1016/j.jtherbio.2021.102858. Epub 2021 Jan 21.
The Asia-Pacific contains over half of the world's population, 21 countries have a Gross Domestic Product <25% of the world's largest economy, many countries have tropical climates and all suffer the impact of global warming. That 'perfect storm' exacerbates the risk of occupational heat illness, yet first responders must perform physically demanding work wearing personal-protective clothing and equipment. Unfortunately, the Eurocentric emphasis of past research has sometimes reduced its applicability to other ethnic groups. To redress that imbalance, relevant contemporary research has been reviewed, to which has been added information applicable to people of Asian, Melanesian and Polynesian ancestry. An epidemiological triad is used to identify the causal agents and host factors of work intolerance within hot-humid climates, commencing with the size dependency of resting metabolism and heat production accompanying load carriage, followed by a progression from the impact of single-layered clothing through to encapsulating ensembles. A morphological hypothesis is presented to account for inter-individual differences in heat production and heat loss, which seems to explain apparent ethnic- and gender-related differences in thermoregulation, at least within thermally compensable states. The mechanisms underlying work intolerance, cardiovascular insufficiency and heat illness are reviewed, along with epidemiological data from the Asia-Pacific. Finally, evidence-based preventative and treatment strategies are presented and updated concerning moisture-management fabrics and barriers, dehydration, pre- and post-exercise cooling, and heat adaptation. An extensive reference list is provided, with >25 recommendations enabling physiologists, occupational health specialists, policy makers, purchasing officers and manufacturers to rapidly extract interpretative outcomes pertinent to the Asia-Pacific.
23Exertional heat stroke in sport and the military: epidemiology and mitigation.PubMed
Julien D Périard, David DeGroot, Ollie Jay
Exp Physiol. 2022 Oct;107(10):1111-1121. doi: 10.1113/EP090686. Epub 2022 Sep 14.
NEW FINDINGS: What is the topic of this review? Exertional heat stroke epidemiology in sport and military settings, along with common risk factors and strategies and policies designed to mitigate its occurrence. What advances does it highlight? Individual susceptibility to exertional heat stroke risk is dependent on the interaction of intrinsic and extrinsic factors. Heat policies in sport should assess environmental conditions, as well as the characteristics of the athlete, clothing/equipment worn and activity level of the sport. Exertional heat stroke risk reduction in the military should account for factors specific to training and personnel. ABSTRACT: Exertional heat illness occurs along a continuum, developing from the relatively mild condition of muscle cramps, to heat exhaustion, and in some cases to the life-threatening condition of heat stroke. The development of exertional heat stroke (EHS) is associated with an increase in core temperature stemming from inadequate heat dissipation to offset the rate of metabolically generated heat. Susceptibility to EHS is linked to the interaction of several factors including environmental conditions, individual characteristics, health conditions, medication and drug use, behavioural responses, and sport/organisational requirements. Two settings in which EHS is commonly observed are competitive sport and the military. In sport, the exact prevalence of EHS is unclear due to inconsistent exertional heat illness terminology, diagnostic criteria and data reporting. In contrast, exertional heat illness surveillance in the military is facilitated by standardised case definitions, a requirement to report all heat illness cases and a centralised medical record repository. To mitigate EHS risk, several strategies can be implemented by athletes and military personnel, including heat acclimation, ensuring adequate hydration, cold-water immersion and mandated work-to-rest ratios. Organisations may also consider developing sport or military task-specific heat stress policies that account for the evaporative heat loss requirement of participants, relative to the evaporative capacity of the environment. This review examines the epidemiology of EHS along with the strategies and policies designed to reduce its occurrence in sport and military settings. We highlight the nuances of identifying individuals at risk of EHS and summarise the benefits and shortcomings of various mitigation strategies.
24Exertional fatigue and cold exposure: mechanisms of hiker's hypothermia.PubMed
Andrew J Young, John W Castellani
Appl Physiol Nutr Metab. 2007 Aug;32(4):793-8. doi: 10.1139/H07-041.
Participants in prolonged, physically demanding activities in cold weather are at risk of a condition known as "hiker's hypothermia". During exposure to cold weather, the increased gradient favoring body heat loss to the environment must be balanced by physiological responses, clothing, and behavioral strategies that conserve body heat stores, or else body temperature will decline. The primary human physiological responses elicited by cold exposure are shivering and peripheral vasoconstriction. Shivering increases thermogenesis and replaces body heat losses, while peripheral vasoconstriction improves thermal insulation of the body and retards the rate of heat loss. A body of scientific literature supports the concept that prolonged and (or) repeated cold exposure, fatigue induced by sustained physical exertion, or both together can impair shivering and vasoconstrictor response to cold. The mechanisms accounting for this thermoregulatory impairment are not clear, but the possibility that changes in blood glucose availability or sympathetic responsiveness to cold due to exertion and fatigue merit further research.
25[Health consequences of environmental temperature and climate variations].PubMed
Bernard Swynghedauw
Bull Acad Natl Med. 2012 Jan;196(1):201-15.
Recent climate change is a consequence of the greenhouse effect and human activity, and is directly responsible for extreme events such as heatwaves (see report of the French Académie des Sciences). Human thermoregulation depends more on behavior than on biology Air conditioning and building structure play an essential role. The 2003 heatwave was not a unique event. Preventive measures reduced mortality during subsequent heatwaves. Most deaths were due to heat stroke associated with dehydration. During strenuous exercise, especially during military training, heat stroke requires specific treatment. Temperature/ global mortality and temperature/cardiovascular mortality curves are both U-shaped. Usually, global mortality increases winter and is linked to temperature. During summer, global mortality increases only when heatwaves occur. Climate change participates in the spread of infectious diseases. Nevertheless, in continental France, for the moment, climate change is not a major factor in the incidence of infectious diseases, despite the fact that several bacteria, viruses and vectors are temperature-sensitive. The situation in Reunion, French Polynesia and French Departments of America is more complicated, due to their geographic heterogeneity. Some areas are more exposed to the climatic risk and could act as a gateway for new infections and mutations. The dramatic loss of biodiversity is partly a consequence of climate change. It increases the transmissibility of some pathogens and can also potentially lead to an increase in autoimmune diseases and obesity. Climate change plays a important role in allergic diseases, through changes in the diffusion and composition of pollens. These modifications are being monitored by several observatories. Six different veterinary diseases, including several zoonoses, are of particular concern.
26Infant death presumably due to exertional self-overheating in bed: an autopsy case of suspected child abuse.PubMed
B L Zhu, K Ishida, M Q Fujita, et al.
Nihon Hoigaku Zasshi. 1998 Apr;52(2):153-6.
We report a case of accidental infant death presumably due to exertional self-overheating in bed. On a winter morning, a 9-month-old female baby was found dead in her bed at home. She had been confined to the bed overnight by her father, totally covered with a blanket and a thick quilt, because her night crying disturbed his sleep. The clothing and bedclothes were extremely wet with sweat. Many petechial hemorrhages were observed in the upper chest and thoracic viscera. The blood was concentrated, indicative of dehydration. Histological and immunohistochemical investigation revealed findings of shock and myolysis in the cardiac and skeletal muscles. There was no evidence of natural diseases. The main cause of death was diagnosed as circulatory collapse from overheating (hyperpyrexia and dehydration; heat stroke/exhaustion) probably precipitated by struggling in the closed space. Although there was no apparent evidence of battering or any other repetitive physical violence, this case was regarded as an atypical type of fatal child abuse.
27[Indoor environment and heatstroke risk].PubMed
Toshiharu Ikaga, Shingo Hori, Yasufumi Miyake, et al.
Nihon Rinsho. 2012 Jun;70(6):1005-12.
This paper describes the outline of heatstroke risk evaluation model for aged residents based on surveys done by the Heatstroke Surveillance Committee of Japanese Association for Acute Medicine and field measurements of indoor air temperature, humidity and so on. To reduce heatstroke of aged residents, promotion of thermal insulation, sun-shading, cross ventilation, air-condition of houses and living behavior of residents are needed.
28[Heatstroke].PubMed
Christophe Bianchi, Laurent Vallotton, Pierre-Nicolas Carron
Praxis (Bern 1994). 2025 Jul;114(7):283-287. doi: 10.23785/PRAXIS.2025.07.005.
Heat stroke is a serious and underdiagnosed condition, which is subdivided into exercise and classic subtypes. Climate change and increasing temperatures are making this pathology more and more common. Its pathophysiology is closely linked to the ability of the cardiovascular system to adapt. Multi-organ damage can complicate this disease, through a systemic inflammatory response. Acute neurological symptoms and signs are the typical clinical presentation of heatstroke. Management is based on early and active cooling, as well as support for vital functions. Preventing this problem requires a community and public health response.
29Thermoregulatory disorders and illness related to heat and cold stress.PubMed
William P Cheshire
Auton Neurosci. 2016 Apr;196:91-104. doi: 10.1016/j.autneu.2016.01.001. Epub 2016 Jan 6.
Thermoregulation is a vital function of the autonomic nervous system in response to cold and heat stress. Thermoregulatory physiology sustains health by keeping body core temperature within a degree or two of 37°C, which enables normal cellular function. Heat production and dissipation are dependent on a coordinated set of autonomic responses. The clinical detection of thermoregulatory impairment provides important diagnostic and localizing information in the evaluation of disorders that impair thermoregulatory pathways, including autonomic neuropathies and ganglionopathies. Failure of neural thermoregulatory mechanisms or exposure to extreme or sustained temperatures that overwhelm the body's thermoregulatory capacity can also result in potentially life-threatening departures from normothermia. Hypothermia, defined as a core temperature of <35.0°C, may present with shivering, respiratory depression, cardiac dysrhythmias, impaired mental function, mydriasis, hypotension, and muscle dysfunction, which can progress to cardiac arrest or coma. Management includes warming measures, hydration, and cardiovascular support. Deaths from hypothermia are twice as frequent as deaths from hyperthermia. Hyperthermia, defined as a core temperature of >40.5°C, may present with sweating, flushing, tachycardia, fatigue, lightheadedness, headache, and paresthesia, progressing to weakness, muscle cramps, oliguria, nausea, agitation, hypotension, syncope, confusion, delirium, seizures, and coma. Mental status changes and core temperature distinguish potentially fatal heat stroke from heat exhaustion. Management requires the immediate reduction of core temperature. Ice water immersion has been shown to be superior to alternative cooling measures. Avoidance of thermal risk and early recognition of cold or heat stress are the cornerstones of preventive therapy.
30Association Between Exercise-Induced Hyperthermia and Intestinal Permeability: A Systematic Review.PubMed
Washington Pires, Christiano E Veneroso, Samuel P Wanner, et al.
Sports Med. 2017 Jul;47(7):1389-1403. doi: 10.1007/s40279-016-0654-2.
BACKGROUND: Prolonged and strenuous physical exercise increases intestinal permeability, allowing luminal endotoxins to translocate through the intestinal barrier and reach the bloodstream. When recognized by the immune system, these endotoxins trigger a systemic inflammatory response that may affect physical performance and, in severe cases, induce heat stroke. However, it remains to be elucidated whether there is a relationship between the magnitude of exercise-induced hyperthermia and changes in intestinal permeability. OBJECTIVE: In this systematic review, we evaluated whether an exercise-induced increase in core body temperature (T ) is associated with an exercise-induced increase in intestinal permeability. METHODS: The present systematic review screened the MEDLINE/PubMed and Web of Science databases in September 2016, without any date restrictions. Sixteen studies that were performed in healthy participants, presented original data, and measured both the exercise-induced changes in T and intestinal permeability were selected. These studies assessed intestinal permeability through the measurement of sugar levels in the urine and measurement of intestinal fatty acid binding protein or lipopolysaccharide levels in the blood. RESULTS: Exercise increased both T and intestinal permeability in most of the 16 studies. In addition, a positive and strong correlation was observed between the two parameters (r = 0.793; p < 0.001), and a T exceeding 39 °C was always associated with augmented permeability. CONCLUSION: The magnitude of exercise-induced hyperthermia is directly associated with the increase in intestinal permeability.
31Heat-related illness.PubMed
Jonathan A Becker, Lynsey K Stewart
Am Fam Physician. 2011 Jun 1;83(11):1325-30.
Heat-related illness is a set of preventable conditions ranging from mild forms (e.g., heat exhaustion, heat cramps) to potentially fatal heat stroke. Hot and humid conditions challenge cardiovascular compensatory mechanisms. Once core temperature reaches 104°F (40°C), cellular damage occurs, initiating a cascade of events that may lead to organ failure and death. Early recognition of symptoms and accurate measurement of core temperature are crucial to rapid diagnosis. Milder forms of heat-related illness are manifested by symptoms such as headache, weakness, dizziness, and an inability to continue activity. These are managed by supportive measures including hydration and moving the patient to a cool place. Hyperthermia and central nervous system symptoms should prompt an evaluation for heat stroke. Initial treatments should focus on lowering core temperature through cold water immersion. Applying ice packs to the head, neck, axilla, and groin is an alternative. Additional measures include transporting the patient to a cool environment, removing excess clothing, and intravenous hydration. Delayed access to cooling is the leading cause of morbidity and mortality in persons with heat stroke. Identification of at-risk groups can help physicians and community health agencies provide preventive measures.
32Rectal and esophageal temperatures during upper- and lower-body exercise.PubMed
E M Gass, G C Gass
Eur J Appl Physiol Occup Physiol. 1998 Jun;78(1):38-42. doi: 10.1007/s004210050384.
This study investigated the question: is core temperature measurement influenced by whether exercise involves predominantly upper- or lower-body musculature? Healthy men were allocated to three groups: treadmill ergometry (T) n = 4, cycle ergometry (C) n = 6 and arm crank ergometry (AC) n = 5. Subjects underwent an incremental exercise test to exhaustion on an exercise-specific ergometer to determine maximum/peak oxygen consumption (VO2max). One week later subjects exercised for 36 min on the same ergometer at approximately 65% VO2max while temperatures at the rectum (T(re)) and esophagus (T(es)) were simultaneously measured. The VO2max (1 x min(-1)) for groups T [4.76 (0.50)] and C [4.35 (0.30)] was significantly higher than that for the AC group [2.61 (0.24)]. At rest, T(re) was significantly higher than T(es) in all groups (P < 0.05). At the end of submaximal exercise in the C group, T(re) [38.32 (0.11) degrees C] was significantly higher than T(es) [38.02 (0.12) degrees C, P < 0.05]. No significant differences between T(re) and T(es) at the end of exercise were noted for AC and T groups. The temperature difference (T(diff)) between T(re) and T(es) was dissimilar at rest in the three groups; however, by the end of exercise T(diff) was approximately 0.2 degrees C for each of the groups, suggesting that at the end of steady-state exercise T(re) can validly be used to estimate core temperature.
33Metabolomic profiling identifies a novel mechanism for heat stroke‑related acute kidney injury.PubMed
Ling Xue, Wenli Guo, Li Li, et al.
Mol Med Rep. 2021 Apr;23(4). doi: 10.3892/mmr.2021.11880. Epub 2021 Jan 28.
Heat stroke can induce a systemic inflammatory response, which may lead to multi‑organ dysfunction including acute kidney injury (AKI) and electrolyte disturbances. To investigate the pathogenesis of heat stroke (HS)‑related AKI, a mouse model of HS was induced by increasing the animal's core temperature to 41˚C. Blood samples obtained from the tail vein were used to measure plasma glucose and creatinine levels. Micro‑positron emission tomography‑computed tomography (micro‑PET/CT), H&E staining and transmission electron microscopy were conducted to examine metabolic and morphological changes in the mouse kidneys. Immunohistochemistry (IHC) and western blot analyses were performed to investigate the expression of apoptosis‑inducing factor mitochondria‑associated 2 (Aifm2), high‑mobility group box 1 (HMGB1) and receptor for advanced glycosylation end products (RAGE). Liquid chromatography‑mass spectrometry analysis was conducted to find differential metabolites and signaling pathways. The HS mouse model was built successfully, with significantly increased creatinine levels detected in the serum of HS mice compared with controls, whereas micro‑PET/CT revealed active metabolism in the whole body of HS mice. H&E and TUNEL staining revealed that the kidneys of HS mice exhibited signs of hemorrhage and apoptosis. IHC and western blotting demonstrated significant upregulation of Aifm2, HMGB1 and RAGE in response to HS. Finally, 136 differential metabolites were screened out, and enrichment of the 'biosynthesis of unsaturated fatty acids' pathway was detected. HS‑associated AKI is the renal manifestation of systemic inflammatory response syndrome, and may be triggered by the HMGB1/RAGE pathway. Metabolomics indicated increased adrenic acid, docosahexaenoic acid and eicosapentaenoic acid may serve as metabolic biomarkers for AKI in HS. The findings suggested that a correlation between the HMGB1/RAGE pathway and biosynthesis of unsaturated fatty acids may contribute to the progression of HS‑related AKI.
34Sports Induced Cardiac Arrest: A Case of Missed Rhabdomyolysis.PubMed
Parshotam L Gautam, Neeru Luthra, Prabhdeep Singh Nain
J Clin Diagn Res. 2015 Sep;9(9):UD01-2. doi: 10.7860/JCDR/2015/10275.6507. Epub 2015 Sep 1.
Exercise induced rhabdomyolysis although uncommon, is well known in strenuous and exhaustive sports like marathons, cycling and wrestlers. But it is not known in Kabaddi players. We report a case of nearly fatal rhabdomyolysis which was missed during early resuscitation in emergency room and lead to cardiac arrest due to catastrophic metabolic acidosis and severe -hyperkalemia. After high quality cardiopulmonary resuscitation and return of spontaneous rhythm, emergency resuscitative exploratory laparotomy was performed for suspected bladder injury which was negative. He had remarkable recovery over 24 h following diagnosis and aggressive supportive management including peritoneal dialysis. Heat stroke and rhabdomyolysis should be suspected early in players playing strenuous sports in tropical countries even during winter. High degree of suspicion and early aggressive general support is the key to success for unusual clinical presentation of any such clinical entity.
35AVE 0991 Attenuates Pyroptosis and Liver Damage after Heatstroke by Inhibiting the ROS-NLRP3 Inflammatory Signalling Pathway.PubMed
Ming Zhang, Xintao Zhu, Huasheng Tong, et al.
Biomed Res Int. 2019 Aug 19;2019:1806234. doi: 10.1155/2019/1806234. eCollection 2019.
We previously demonstrated that angiotensin-(1-7) (Ang-(1-7)), an essential endocrine factor, inhibits the NLRP3 inflammasome by regulating reactive oxygen species (ROS) in fibrotic livers. We also demonstrated that the NLRP3 inflammasome contributes to the liver damage induced by pyroptosis after heatstroke. However, the role of Ang-(1-7) in the hepatocytes under heat stress remains uncertain. We aimed to examine the change in angiotensin peptides in the livers affected by heatstroke and the effect on the ROS-NLRP3 inflammatory signalling pathway. , increased angiotensin II (Ang II) and decreased Ang-(1-7) in the serum of heatstroke patients suffering from hepatic dysfunction were observed. The change in angiotensin peptides was considered a potential biomarker that could be used to predict hepatic dysfunction. Enhanced Ang II and attenuated Ang-(1-7) levels were also observed in the liver tissue of heatstroke rats, which were consistent with their receptors and converting enzymes. Hepatic damage associated with increased ROS and protein expression levels of NOX4, NLRP3, caspase-1, and IL-1 was attenuated by AVE 0991, an analogue of Ang-(1-7). , pyroptosis, characterized by activated caspase-1 and IL-1, was observed in hepatocytes under heat stress, which was enhanced by Ang II and attenuated by antioxidants, NOX4 siRNA, and AVE 0991. In summary, AVE 0991 attenuates pyroptosis and liver damage induced by heat stress by inhibiting the ROS-NLRP3 inflammatory signalling pathway.
36An autopsy case of infant death due to heat stroke.PubMed
T Ohshima, H Maeda, T Takayasu, et al.
Am J Forensic Med Pathol. 1992 Sep;13(3):217-21. doi: 10.1097/00000433-199209000-00010.
We report an autopsy case of infant death due to heat stroke. On a winter day, a 52-day-old female baby was placed under a Japanese electric foot warmer with a coverlet (kotatsu) on an electric carpet warmer in a heated room at home. After about 5 h, the mother noticed that the baby was unconscious and took her to a hospital. Spontaneous respiration, however, was already absent, and the pupils were dilated. The trunk was hot; body temperature was 41.3 degrees C. The skin of the whole body was dry. Autopsy revealed second-degree burn injuries on the left side of the face and the dorsum of the left hand. Numerous marked petechiae and ecchymoses were found in the thymus (capsule and parenchyma), pleurae (visceral and parietal), pericardial cavity (internal and external surfaces), epicardium, and beneath the serosa at the origin of the aorta. In addition, there was congestion in various organs, edema in the brain and lungs, and hemorrhage in the lungs. Histopathologically, macrophages without hemosiderin granules were present in the alveoli. When the heating conditions at the accident were reproduced experimentally, the temperature in the electric kotatsu warmer rose to 50-60 degrees C. Thus, we concluded that misuse of the electric kotatsu caused heat stroke in this infant.
37Consensus Statement- Prehospital Care of Exertional Heat Stroke.PubMed
Luke N Belval, Douglas J Casa, William M Adams, et al.
Prehosp Emerg Care. 2018 May-Jun;22(3):392-397. doi: 10.1080/10903127.2017.1392666. Epub 2018 Jan 16.
Exertional heat stroke (EHS) is one of the most common causes of sudden death in athletes. It also represents a unique medical challenge to the prehospital healthcare provider due to the time sensitive nature of treatment. In cases of EHS, when cooling is delayed, there is a significant increase in organ damage, morbidity, and mortality after 30 minutes, faster than the average EMS transport and ED evaluation window. The purpose of this document is to present a paradigm for prehospital healthcare systems to minimize the risk of morbidity and mortality for EHS patients. With proper planning, EHS can be managed successfully by the prehospital healthcare provider.
38First aid cooling techniques for heat stroke and exertional hyperthermia: A systematic review and meta-analysis.PubMed
Matthew J Douma, Theresa Aves, Katherine S Allan, et al.
Resuscitation. 2020 Mar 1;148:173-190. doi: 10.1016/j.resuscitation.2020.01.007. Epub 2020 Jan 22.
BACKGROUND: Heat stroke is an emergent condition characterized by hyperthermia (>40 °C/>104 °F) and nervous system dysregulation. There are two primary etiologies: exertional which occurs during physical activity and non-exertional which occurs during extreme heat events without physical exertion. Left untreated, both may lead to significant morbidity, are considered a special circumstance for cardiac arrest, and cause of mortality. METHODS: We searched Medline, Embase, CINAHL and SPORTDiscus. We used Grading of Recommendations Assessment, Development and Evaluation (GRADE) methods and risk of bias assessments to determine the certainty and quality of evidence. We included randomized controlled trials, non-randomized trials, cohort studies and case series of five or more patients that evaluated adults and children with non-exertional or exertional heat stroke or exertional hyperthermia, and any cooling technique applicable to first aid and prehospital settings. Outcomes included: cooling rate, mortality, neurological dysfunction, adverse effects and hospital length of stay. RESULTS: We included 63 studies, of which 37 were controlled studies, two were cohort studies and 24 were case series of heat stroke patients. Water immersion of adults with exertional hyperthermia [cold water (14-17 °C/57.2-62.6 °F), colder water (8-12 °C/48.2-53.6 °F) and ice water (1-5 °C/33.8-41 °F)] resulted in faster cooling rates when compared to passive cooling. No single water temperature range was found to be associated with a quicker core temperature reduction than another (cold, colder or ice). CONCLUSION: Water immersion techniques (using 1-17 °C water) more effectively lowered core body temperatures when compared with passive cooling, in hyperthermic adults. The available evidence suggests water immersion can rapidly reduce core body temperature in settings where it is feasible.
39Cooling methods used in the treatment of exertional heat illness.PubMed
J E Smith
Br J Sports Med. 2005 Aug;39(8):503-7; discussion 507. doi: 10.1136/bjsm.2004.013466.
OBJECTIVE: To review the different methods of reducing body core temperature in patients with exertional heatstroke. METHODS: The search strategy included articles from 1966 to July 2003 using the databases Medline and Premedline, Embase, Evidence Based Medicine (EBM) reviews, SPORTDiscus, and cross referencing the bibliographies of relevant papers. Studies were included if they contained original data on cooling times or cooling rates in patients with heat illness or normal subjects who were subjected to heat stress. RESULTS: In total, 17 papers were included in the analysis. From the evidence currently available, the most effective method of reducing body core temperature appears to be immersion in iced water, although the practicalities of this treatment may limit its use. Other methods include both evaporative and invasive techniques, and the use of chemical agents such as dantrolene. CONCLUSIONS: The main predictor of outcome in exertional heatstroke is the duration and degree of hyperthermia. Where possible, patients should be cooled using iced water immersion, but, if this is not possible, a combination of other techniques may be used to facilitate rapid cooling. There is no evidence to support the use of dantrolene in these patients. Further work should include a randomised trial comparing immersion and evaporative therapy in heatstroke patients.
40Society of Critical Care Medicine Guidelines for the Treatment of Heat Stroke.PubMed
Jeffrey F Barletta, Tina L Palmieri, Shari A Toomey, et al.
Crit Care Med. 2025 Feb 1;53(2):e490-e500. doi: 10.1097/CCM.0000000000006551. Epub 2025 Feb 21.
RATIONALE: Predicted increases in heat-related weather phenomena will result in increasing heat exposures and heat injuries, like heat stroke. Prompt recognition, early intervention, and evidence-based management are necessary to optimize outcomes. OBJECTIVES: The objective of these guidelines was to develop evidence-based recommendations for the treatment of patients with heat stroke. DESIGN: The Society of Critical Care Medicine convened a multidisciplinary panel of 18 international clinicians, comprising expertise in critical care, emergency medicine, neurocritical care, surgery, trauma/burn surgery, sports medicine, athletic training, military medicine, nursing, pharmacy, respiratory therapy, and one patient representative. The panel also included a guidelines methodologist specialized in developing evidence-based recommendations in alignment with the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) methodology. Conflict-of-interest policies were strictly followed during all phases of guidelines development including panel selection and voting. METHODS: The panel members identified Patient, Intervention, Comparison, and Outcomes questions in two main areas: cooling modalities and medications that affect temperature. A systematic review for each question was conducted to identify the best available evidence, statistically analyze the evidence, and assess the certainty of the evidence using the GRADE methodology. The GRADE evidence-to-decision framework was used to formulate the recommendations. Good practice statements were included to provide additional clinical guidance. RESULTS: The panel generated two strong recommendations, five good practice statements and one "only-in-the-context of research" statement. Active cooling measures are recommended over passive cooling methods, with cold- or ice-water immersion achieving the fastest cooling rate. This method should be prioritized where available. In heat stroke patients, there is no evidence to support pharmacological interventions that affect temperature control and they should be avoided. CONCLUSIONS: The guidelines task force provided recommendations for the management of patients with heat stroke. These recommendations should be considered along with the patient's clinical status and available resources.
41The pathogenesis and therapeutic strategies of heat stroke-induced liver injury.PubMed
Fuquan Wang, Yan Zhang, Jianhua Li, et al.
Crit Care. 2022 Dec 17;26(1):391. doi: 10.1186/s13054-022-04273-w.
Heat stroke (HS) is a life-threatening systemic disease characterized by an elevated core body temperature of more than 40 ℃ and subsequent multiple organ dysfunction syndrome. With the growing frequency of global heatwaves, the incidence rate of HS has increased significantly, which has caused a huge burden on people's lives and health. Liver injury is a well-documented complication of HS and usually constitutes the direct cause of patient death. In recent years, a lot of research has been carried out on the pathogenesis and treatment strategies of HS-induced liver injury. In this review, we summarized the important pathogenesis of HS-induced liver injury that has been confirmed so far. In addition to the comprehensive effect of systemic factors such as heat cytotoxicity, coagulopathy, and systemic inflammatory response syndrome, excessive hepatocyte cell pyroptosis, dysfunction of Kupffer cells, abnormal expression of heat shock protein expression, and other factors are also involved in the pathogenesis of HS-induced liver injury. Furthermore, we have also established the current therapeutic strategies for HS-induced liver injury. Our study is of great significance in promoting the understanding of the pathogenesis and treatment of HS-induced liver injury.
42[Research progress in the multiple organ dysfunction syndrome caused by heat stroke].PubMed
Mengmeng Yang, Yu Zhang, Yan Zhao, et al.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2017 Feb;29(2):188-192. doi: 10.3760/cma.j.issn.2095-4352.2017.02.020.
Heat stroke (HS) is a life-threatening illness characterized by core body temperatures above 40 °C coupled with central nervous system (CNS) dysfunction, including delirium, convulsions, and/or coma. Its morbidity has increased dramatically in the past few decades. Multiple organ dysfunction syndrome (MODS) is not only the most serious complication of HS, but also the leading cause of deaths. Understanding the pathogenesis, characteristic and advancement pattern of MODS caused by HS will have a profound effect on the clinical treatment, research and mortality decrease. The pathogenesis, injury characteristic of each system and organ, and treatment methods were summarized in this review so as to deepen the clinical recognition of this disease.
43[Pathophysiology and management of heat illness].PubMed
Thomas Bein
Med Klin Intensivmed Notfmed. 2024 Jun;119(5):373-380. doi: 10.1007/s00063-023-01072-1. Epub 2023 Oct 13.
BACKGROUND: The frequency and intensity of heat waves are currently increasing due to climate change. Hence more cases of heat illness are being observed, a potentially life-threatening disease, which requires rapid and expert management. OBJECTIVES: An overview of the pathophysiology and acute management of heat illness is presented. MATERIALS AND METHODS: Analysis and evaluation of important, recently published contributions, studies, and reviews regarding heat illness without claim for completeness or fulfilling the criteria for a 'systematic meta-analysis'. Presentation of a recommended clinical-practical classification and management of heat illness in emergency departments or intensive care units. RESULTS: The manifestation of heat illness arising from prolonged exposure to heat prevaries (heat cramps, heat edema, heat exhaustion, heat stroke). The main pathophysiologic mechanisms are disruption of thermoregulation, peripheral vasodilation of the skin surface, hypoperfusion of visceral organs, and brain, and cardiac stress. Uncompensated heat stress can result in multiorgan dysfunction/failure syndrome due to the initiation of cytokine pathways, specifically in at-risk and/or chronically ill patients. The manifestation of uncompensated heat stroke is associated with a hospital mortality > 50%. Rapid identification, classification and targeted management are crucial for the outcome, in particular the initiation of adequate cooling measures. CONCLUSION: In the future, increasing numbers of patients suffering from prolonged heat exposure will require treatment in emergency departments and intensive care units. Sufficient professional knowledge regarding pathophysiology and management are decisive for successful therapy. Hence, the topic heat illness should be implemented in training and education.
44Evidence-Based Heatstroke Management in the Emergency Department.PubMed
Caitlin Rublee, Caleb Dresser, Catharina Giudice, et al.
West J Emerg Med. 2021 Feb 26;22(2):186-195. doi: 10.5811/westjem.2020.11.49007.
INTRODUCTION: Climate change is causing an increase in the frequency and intensity of extreme heat events, which disproportionately impact the health of vulnerable populations. Heatstroke, the most serious heat-related illness, is a medical emergency that causes multiorgan failure and death without intervention. Rapid recognition and aggressive early treatment are essential to reduce morbidity and mortality. The objective of this study was to evaluate current standards of care for the emergent management of heatstroke and propose an evidence-based algorithm to expedite care. METHODS: We systematically searched PubMed, Embase, and key journals, and reviewed bibliographies. Original research articles, including case studies, were selected if they specifically addressed the recognition and management of heatstroke in any prehospital, emergency department (ED), or intensive care unit population. Reviewers evaluated study quality and abstracted information regarding demographics, scenario, management, and outcome. RESULTS: In total, 63 articles met full inclusion criteria after full-text review and were included for analysis. Three key themes identified during the qualitative review process included recognition, rapid cooling, and supportive care. Rapid recognition and expedited external or internal cooling methods coupled with multidisciplinary management were associated with improved outcomes. Delays in care are associated with adverse outcomes. We found no current scalable ED alert process to expedite early goal-directed therapies. CONCLUSION: Given the increased risk of exposure to heat waves and the time-sensitivity of the condition, EDs and healthcare systems should adopt processes for rapid recognition and management of heatstroke. This study proposes an evidence-based prehospital and ED heat alert pathway to improve early diagnosis and resource mobilization. We also provide an evidence-based treatment pathway to facilitate efficient patient cooling. It is hoped that this protocol will improve care and help healthcare systems adapt to changing environmental conditions.
45The significant mechanism and treatments of cell death in heatstroke.PubMed
Zixin Wang, Jie Zhu, Dingshun Zhang, et al.
Apoptosis. 2024 Aug;29(7-8):967-980. doi: 10.1007/s10495-024-01979-w. Epub 2024 Jun 17.
With global warming, extreme environmental heat is becoming a social issue of concern, which can cause adverse health results including heatstroke (HS). Severe heat stress is characterized by cell death of direct heat damage, excessive inflammatory responses, and coagulation disorders that can lead to multiple organ dysfunction (MODS) and even death. However, the significant pathophysiological mechanism and treatment of HS are still not fully clear. Various modes of cell death, including apoptosis, pyroptosis, ferroptosis, necroptosis and PANoptosis are involved in MODS induced by heatstroke. In this review, we summarized molecular mechanism, key transcriptional regulation as for HSF1, NRF2, NF-κB and PARP-1, and potential therapies of cell death resulting in CNS, liver, intestine, reproductive system and kidney injury induced by heat stress. Understanding the mechanism of cell death provides new targets to protect multi-organ function in HS.
46Dexamethasone improves heat stroke-induced multiorgan dysfunction and damage in rats.PubMed
Chia-Chyuan Liu, Mei-Fen Shih, Yi-Szu Wen, et al.
Int J Mol Sci. 2014 Nov 18;15(11):21299-313. doi: 10.3390/ijms151121299.
Dexamethasone (DXM) is known as an immunosuppressive drug used for inflammation control. In the present study, we attempted to examine whether DXM administration could attenuate the hypercoagulable state and the overproduction of pro-inflammatory cytokines, improve arterial hypotension, cerebral ischemia and damage, and vital organ failure in a rat model of heat stroke. The results indicated that all the rats suffering from heat stroke showed high serum levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), accompanied with increased prothrombin time, activated partial thromboplastin time and D-D dimer, and decreased protein C. During the induction period of heat stroke, plasma levels of blood urea nitrogen (BUN), creatinine, glutamic oxaloacetic transaminase (SGOT), glutamic pyruvic transaminase (SGPT), and alkaline phosphatase (ALP), were consistently increased. High striatal levels of glycerol, glutamate, and lactate/pyruvate were simultaneously detected. On the contrary, the mean arterial pressure, plasma levels of interleukin-10 (IL-10), and local cerebral blood flow at the striatum were all decreased. Importantly, intravenous administration of DXM substantially ameliorated the circulatory dysfunction, systematic inflammation, hypercoagulable state, cerebral ischemia and damage during the induction period of heat stroke. These findings demonstrated that DXM may be an alternative therapy that can ameliorate heat stroke victims by attenuating activated coagulation, systemic inflammation, and vital organ ischemia/injury during heat stroke.
47Altitude training considerations for the winter sport athlete.PubMed
Robert F Chapman, Jonathon L Stickford, Benjamin D Levine
Exp Physiol. 2010 Mar;95(3):411-21. doi: 10.1113/expphysiol.2009.050377. Epub 2009 Oct 16.
Winter sports events routinely take place at low to moderate altitudes, and nearly all Winter Olympic Games have had at least one venue at an altitude >1000 m. The acute and chronic effects of altitude can have a substantial effect on performance outcomes. Acutely, the decline in oxygen delivery to working muscle decreases maximal oxygen uptake, negatively affecting performance in endurance events, such as cross-country skiing and biathlon. The reduction in air resistance at altitude can dramatically affect sports involving high velocities and technical skill components, such as ski jumping, speed skating, figure skating and ice hockey. Dissociation between velocity and sensations usually associated with work intensity (ventilation, metabolic signals in skeletal muscle and heart rate) may impair pacing strategy and make it difficult to determine optimal race pace. For competitions taking place at altitude, a number of strategies may be useful, depending on the altitude of residence of the athlete and ultimate competition altitude, as follows. First, allow extra time and practice (how much is yet undetermined) for athletes to adjust to the changes in projectile motion; hockey, shooting, figure skating and ski jumping may be particularly affected. These considerations apply equally in the reverse direction; that is, for athletes practising at altitude but competing at sea level. Second, allow time for acclimatization for endurance sports: 3-5 days if possible, especially for low altitude (500-2000 m); 1-2 weeks for moderate altitude (2000-3000 m); and at least 2 weeks if possible for high altitude (>3000 m). Third, increase exercise-recovery ratios as much as possible, with 1:3 ratio probably optimal, and consider more frequent substitutions for sports where this is allowed, such as ice hockey. Fourth, consider the use of supplemental O(2) on the sideline (ice hockey) or in between heats (skating and Alpine skiing) to facilitate recovery. For competitions at sea level, the 'live high-train low' model of altitude training can help athletes in endurance events to maximize performance.
48Application of altitude/hypoxic training by elite athletes.PubMed
Randall L Wilber
Med Sci Sports Exerc. 2007 Sep;39(9):1610-24. doi: 10.1249/mss.0b013e3180de49e6.
At the Olympic level, differences in performance are typically less than 0.5%. This helps explain why many contemporary elite endurance athletes in summer and winter sport incorporate some form of altitude/hypoxic training within their year-round training plan, believing that it will provide the "competitive edge" to succeed at the Olympic level. The purpose of this paper is to describe the practical application of altitude/hypoxic training as used by elite athletes. Within the general framework of the paper, both anecdotal and scientific evidence will be presented relative to the efficacy of several contemporary altitude/hypoxic training models and devices currently used by Olympic-level athletes for the purpose of legally enhancing performance. These include the three primary altitude/hypoxic training models: 1) live high+train high (LH+TH), 2) live high+train low (LH+TL), and 3) live low+train high (LL+TH). The LH+TL model will be examined in detail and will include its various modifications: natural/terrestrial altitude, simulated altitude via nitrogen dilution or oxygen filtration, and hypobaric normoxia via supplemental oxygen. A somewhat opposite approach to LH+TL is the altitude/hypoxic training strategy of LL+TH, and data regarding its efficacy will be presented. Recently, several of these altitude/hypoxic training strategies and devices underwent critical review by the World Anti-Doping Agency (WADA) for the purpose of potentially banning them as illegal performance-enhancing substances/methods. This paper will conclude with an update on the most recent statement from WADA regarding the use of simulated altitude devices.
49Practical Hydration Solutions for Sports.PubMed
Luke N Belval, Yuri Hosokawa, Douglas J Casa, et al.
Nutrients. 2019 Jul 9;11(7):1550. doi: 10.3390/nu11071550.
Personalized hydration strategies play a key role in optimizing the performance and safety of athletes during sporting activities. Clinicians should be aware of the many physiological, behavioral, logistical and psychological issues that determine both the athlete's fluid needs during sport and his/her opportunity to address them; these are often specific to the environment, the event and the individual athlete. In this paper we address the major considerations for assessing hydration status in athletes and practical solutions to overcome obstacles of a given sport. Based on these solutions, practitioners can better advise athletes to develop practices that optimize hydration for their sports.
50International Society of Sports Nutrition Position Stand: nutritional considerations for single-stage ultra-marathon training and racing.PubMed
Nicholas B Tiller, Justin D Roberts, Liam Beasley, et al.
J Int Soc Sports Nutr. 2019 Nov 7;16(1):50. doi: 10.1186/s12970-019-0312-9.
Background In this Position Statement, the International Society of Sports Nutrition (ISSN) provides an objective and critical review of the literature pertinent to nutritional considerations for training and racing in single-stage ultra-marathon. Recommendations for Training. i) Ultra-marathon runners should aim to meet the caloric demands of training by following an individualized and periodized strategy, comprising a varied, food-first approach; ii) Athletes should plan and implement their nutrition strategy with sufficient time to permit adaptations that enhance fat oxidative capacity; iii) The evidence overwhelmingly supports the inclusion of a moderate-to-high carbohydrate diet (i.e., ~ 60% of energy intake, 5-8 g·kg·d) to mitigate the negative effects of chronic, training-induced glycogen depletion; iv) Limiting carbohydrate intake before selected low-intensity sessions, and/or moderating daily carbohydrate intake, may enhance mitochondrial function and fat oxidative capacity. Nevertheless, this approach may compromise performance during high-intensity efforts; v) Protein intakes of ~ 1.6 g·kg·d are necessary to maintain lean mass and support recovery from training, but amounts up to 2.5 g.kg·d may be warranted during demanding training when calorie requirements are greater; Recommendations for Racing. vi) To attenuate caloric deficits, runners should aim to consume 150-400 Kcal·h (carbohydrate, 30-50 g·h; protein, 5-10 g·h) from a variety of calorie-dense foods. Consideration must be given to food palatability, individual tolerance, and the increased preference for savory foods in longer races; vii) Fluid volumes of 450-750 mL·h (~ 150-250 mL every 20 min) are recommended during racing. To minimize the likelihood of hyponatraemia, electrolytes (mainly sodium) may be needed in concentrations greater than that provided by most commercial products (i.e., > 575 mg·L sodium). Fluid and electrolyte requirements will be elevated when running in hot and/or humid conditions; viii) Evidence supports progressive gut-training and/or low-FODMAP diets (fermentable oligosaccharide, disaccharide, monosaccharide and polyol) to alleviate symptoms of gastrointestinal distress during racing; ix) The evidence in support of ketogenic diets and/or ketone esters to improve ultra-marathon performance is lacking, with further research warranted; x) Evidence supports the strategic use of caffeine to sustain performance in the latter stages of racing, particularly when sleep deprivation may compromise athlete safety.
51Nutritional Strategies to Optimize Performanceand Recovery in Rowing Athletes.PubMed
Jooyoung Kim, Eun-Kyung Kim
Nutrients. 2020 Jun 5;12(6):1685. doi: 10.3390/nu12061685.
Rowing is a high-intensity sport requiring a high level of aerobic and anaerobic capacity. Although good nutrition is essential for successful performance in a rowing competition, its significance is not sufficiently established. This review aimed to provide nutritional strategies to optimize performance and recovery in rowing athletes based on a literature review. Following the guidelines given in the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA), we performed web searches using online databases (Pubmed, Web of Science, Wiley Online Library, ACS Publications, and SciFinder). Typically, a rowing competition involves a 6-8-min high-intensity exercise on a 2000-m course. The energy required for the exercise is supplied by muscle-stored glycogens, which are derived from carbohydrates. Therefore, rowing athletes can plan their carbohydrate consumption based on the intensity, duration, and type of training they undergo. For effective and safe performance enhancement, rowing athletes can take supplements such as β-alanine, caffeine, β-hydroxy-β-methylbutyric acid (HMB), and beetroot juice (nitrate). An athlete may consume carbohydrate-rich foods or use a carbohydrate mouth rinse. Recovery nutrition is also very important to minimize the risk of injury or unexplained underperformance syndrome (UUPS) from overuse. It must take into account refueling (carbohydrate), rehydration (fluid), and repair (protein). As lightweight rowing athletes often attempt acute weight loss by limiting food and fluid intake to qualify for a competition, they require personalized nutritional strategies and plans based on factors such as their goals and environment. Training and competition performance can be maximized by including nutritional strategies in training plans.
52Health Risk Assessment Based on Exposure to Chemicals in Air.PubMed
Hironari Sakamoto, Shigehisa Uchiyama, Ayana Sato, et al.
Int J Environ Res Public Health. 2022 Nov 28;19(23):15813. doi: 10.3390/ijerph192315813.
Few studies have investigated personal exposure concentrations of not only some volatile organic compounds but also more types of chemicals including acidic gases and acrolein. We measured the personal exposure concentrations of 35 chemicals including these chemicals in indoor and outdoor air in Chiba-shi, Japan, for 7 days in summer and winter to assess the associated health risks in 22 people. The personal exposure concentrations of nitrogen dioxide were higher in winter than in summer, and those of formaldehyde, -dichlorobenzene, and tetradecane were higher in summer than in winter. The personal exposure concentrations were mostly equal to or lower than the concentrations in indoor air, contrary to the results of a lot of previous studies. The high-risk chemicals based on personal exposure concentrations were identified as acrolein (max. 0.43 μg/m), benzene (max. 3.1 μg/m), and hexane (max. 220 μg/m) in summer, and acrolein (max. 0.31 μg/m), nitrogen dioxide (max. 320 μg/m), benzene (max. 5.2 μg/m), formic acid (max. 70 μg/m), and hexane (max. 290 μg/m) in winter. In addition, we estimated personal exposure concentrations according to the time spent at home and the chemical concentrations in indoor and outdoor air. We found that the estimated concentrations of some participants largely differed from the measured ones indicating that it is difficult to estimate personal exposure concentrations based on only these data.
53Environmental risk assessment and concentration trend of atmospheric volatile organic compounds in Hyogo Prefecture, Japan.PubMed
Yasushi Okada, Akihiro Nakagoshi, Masahiro Tsurukawa, et al.
Environ Sci Pollut Res Int. 2012 Jan;19(1):201-13. doi: 10.1007/s11356-011-0550-0. Epub 2011 Jun 30.
PURPOSE: The purpose of this study was to evaluate the influences of volatile organic compounds (VOCs) emissions on hazardousness and photochemical reactivity and to propose efficient VOCs abatement strategies. METHODS: The atmospheric concentrations of 101 components of VOCs were measured at six sites which comprehend four urban areas, a roadside area, and an industrial area in Hyogo Prefecture. VOCs influence on hazardousness and photochemical reactivity were evaluated using VOCs measured data and the index on the health effect evaluation and ozone formation potential. The substances that require emissions reduction were selected from the evaluation results. The state and characteristics of environmental pollution were considered from the concentration trends of the selected substances. RESULTS: In industrial area, n-hexadecane, styrene, vinyl chloride monomer, and 1,2-dichloroethane showed a high concentration. In roadside area, n-hexane, n-undecane, n-dodecane, tetrachloroethylene, formaldehyde, acetaldehyde, and 1-butanol showed a high concentration. The excess cancer incidences for formaldehyde exceeded 10(-5) of the level of concern for carcinogenic effect at all sites. Toluene had a high percentage of ozone production. The interannual and seasonal trends of toluene concentrations were different at a regional level and the formaldehyde concentrations in summer were significantly higher than those in winter at the urban sites. CONCLUSIONS: The results show the need to prepare the emission reduction plan for the major sources such as vehicle exhaust, solvent use, and industrial processes to diminish the concentration of toluene that contributes significantly to the formation of photochemical oxidant.
54Occurrence and risk assessment of PAHs from athletic fields under typical rainfall events.PubMed
Xiaoran Zhang, Yuyang Gu, Yinrui Wang, et al.
Water Sci Technol. 2023 May;87(9):2159-2171. doi: 10.2166/wst.2023.092.
Six polycyclic aromatic hydrocarbons (PAHs) including naphthalene (Nap), fluorene (Flu), phenanthrene (Phe), fluoranthene (Fla), pyrene (Pyr), and chrysene (Chr) were detected in runoff from five athletic fields during three rainfall events. The event mean concentration (EMC) of ∑PAHs ranged from 3.96 to 23.23 μg/L, which was much higher than the EMC in urban traffic area runoff. Except for Nap, the PAH concentrations followed in the order of artificial turf > badminton court > basketball court > plastic runway > optennis court. The surface characteristics of the athletic fields, such as the composition of materials and roughness, played an essential role in the release of PAHs. ∑PAHs concentration during the 2nd rainfall event (July 22nd) was the highest among the three rainfall events, indicating that high rainfall intensity facilitated the PAHs release. PAHs during three rainfall events showed little first flush effect except for the artificial turf during the 2nd (22nd July) and 3rd (29th July) rainfall events. The first flush effect could be affected by rainfall characters, PAH properties, and surface characteristics of athletic fields. Ecological risk assessment showed that PAHs in runoff corresponded to moderate-to-high risk, while health risk assessment showed that PAHs could pose a potential carcinogenic danger to human health via dermal contact.
55Synthetic Turf Fields, Crumb Rubber, and Alleged Cancer Risk.PubMed
Archie Bleyer
Sports Med. 2017 Dec;47(12):2437-2441. doi: 10.1007/s40279-017-0735-x.
Most synthetic turf fields have crumb rubber interspersed among the simulated grass fibers to reduce athletic injuries by allowing users to turn and slide more readily as they play sports or exercise on the fields. Recently, the crumbs have been implicated in causing cancer in adolescents and young adults who use the fields, particularly lymphoma and primarily in soccer goalkeepers. This concern has led to the initiation of large-scale studies by local and federal governments that are expected to take years to complete. Meanwhile, should the existing synthetic turf fields with crumb rubber be avoided? What should parents, players, coaches, school administrators, and playground developers do? What should sports medicine specialists and other health professionals recommend? Use grass fields when weather and field conditions permit? Exercise indoors? Three basic premises regarding the nature of the reported cancers, the latency of exposure to environmental causes of cancer to the development of clinically detectable cancer, and the rarity of environmental causation of cancer in children, adolescents, and young adults suggest otherwise.
56Exertional heat stroke: an evidence based approach to clinical assessment and management.PubMed
David W DeGroot, Francis G O'Connor, William O Roberts
Exp Physiol. 2022 Oct;107(10):1172-1183. doi: 10.1113/EP090488. Epub 2022 Jul 13.
NEW FINDINGS: What is the topic of this review? The treatment of exertional heat stress, from initial field care through the return-to-activity decision. What advances does it highlight? Clinical assessment during field care using AVPU and vital signs to gauge recovery, approaches to field cooling and end of active cooling, and shared clinical decision making for return to activity recommendations. ABSTRACT: Exertional heat stroke (EHS) is a potentially fatal condition characterized by central nervous system (CNS) dysfunction and body temperature often but not always >40°C that occurs in the context of physical work in warm or hot environments. In this paper, we review the continuum of care, from initial recognition and field care to transport and hospital care, and finally return-to-duty considerations. Morbidity and mortality can be greatly reduced if not eliminated with prompt recognition and aggressive cooling. If medical personnel are not present at point of collapse during or immediately following exercise, EHS should be the presumptive diagnosis until a formal diagnosis can be determined by qualified medical staff. EHS is a rare medical situation where initial treatment (cooling) takes precedence over transport to a medical facility, where advanced medical care may be required for severe EHS casualties. Recovery from EHS and return to activity is usually straightforward and unremarkable provided the casualty is rapidly cooled at time of collapse and adequate time is allowed for body healing. However, evidence-based data to guide return to activity following EHS are limited. Current research suggests that most individuals recover completely within a few weeks though some individuals may suffer prolonged sequalae and additional evaluation may be warranted, including heat tolerance testing (HTT). Several aspects of the care of the EHS casualty are based on best practices derived from personal experience and continued research is necessary to optimize evaluation and management.
57What every intensivist should know about exertional heat stroke.PubMed
Niccolò Stomeo, Laura Leuci, Paolo Emilio Adami, et al.
J Crit Care. 2025 Oct;89:155134. doi: 10.1016/j.jcrc.2025.155134. Epub 2025 Jun 3.
Exertional heat stroke (EHS) is a life-threatening condition caused by strenuous physical activity, leading to severe hyperthermia and central nervous system dysfunction. Unlike classic heat stroke, EHS can occur in young, healthy individuals and in temperate climates, when heat production exceeds the body's ability to dissipate heat. Rising global temperatures and increased participation in endurance events are contributing to a growing incidence of EHS. Early recognition and rapid cooling are essential to prevent multi-organ failure and death. Whole-body cold-water immersion is the gold standard treatment, and the principle of "cool first, transport second" is key to improving survival. In-hospital care focuses on continued cooling when necessary and managing complications such as acute kidney injury, coagulopathy, liver dysfunction, and neurological impairment. This review provides intensivists with practical guidance on the pathophysiology, diagnosis, and management of EHS. Given their expertise in critical illness and involvement in prehospital and emergency care, intensivists play a pivotal role in early intervention and reducing morbidity and mortality. As EHS incidence rises, increased awareness and preparedness are essential to ensure timely, effective treatment and improve patient outcomes.
58Effects of extreme temperatures on cardiovascular emergency hospitalizations in a Mediterranean region: a self-controlled case series study.PubMed
Anna Ponjoan, Jordi Blanch, Lia Alves-Cabratosa, et al.
Environ Health. 2017 Apr 4;16(1):32. doi: 10.1186/s12940-017-0238-0.
BACKGROUND: Cold spells and heatwaves increase mortality. However little is known about the effect of heatwaves or cold spells on cardiovascular morbidity. This study aims to assess the effect of cold spells and heatwaves on cardiovascular diseases in a Mediterranean region (Catalonia, Southern Europe). METHODS: We conducted a population-based retrospective study. Data were obtained from the System for the Development of Research in Primary Care and from the Catalan Meteorological Service. The outcome was first emergency hospitalizations due to coronary heart disease, stroke, or heart failure. Exposures were: cold spells; cold spells and 3 or 7 subsequent days; and heatwaves. Incidence rate ratios (IRR) and 95% confidence intervals were calculated using the self-controlled case series method. We accounted for age, time trends, and air pollutants; results were shown by age groups, gender or cardiovascular event type. RESULTS: There were 22,611 cardiovascular hospitalizations in winter and 17,017 in summer between 2006 and 2013. The overall incidence of cardiovascular hospitalizations significantly increased during cold spells (IRR = 1.120; CI 95%: 1.10-1.30) and the effect was even stronger in the 7 days subsequent to the cold spell (IRR = 1.29; CI 95%: 1.22-1.36). Conversely, cardiovascular hospitalizations did not increase during heatwaves, neither in the overall nor in the stratified analysis. CONCLUSIONS: Cold spells but not heatwaves, increased the incidence of emergency cardiovascular hospitalizations in Catalonia. The effect of cold spells was greater when including the 7 subsequent days. Such knowledge might be useful to develop strategies to reduce the impact of extreme temperature episodes on human health.
59Physical Activity, a Critical Exposure Factor of Environmental Pollution in Children and Adolescents Health Risk Assessment.PubMed
Jingmei Dong, Su Zhang, Li Xia, et al.
Int J Environ Res Public Health. 2018 Jan 23;15(2):176. doi: 10.3390/ijerph15020176.
It is an extremely urgent problem that physical fitness promotion must face not only the increasing air pollution but also the decline of physical activity level of children and adolescents worldwide at present, which is the major reason that forms an inactive lifestyle and does harm to adolescents' health. Thus, it is necessary to focus on the exposure factor in environmental health risk assessment (EHRA) which conducts supervision of environmental pollution and survey of adolescents' activity patterns according to the harmful characteristics of air pollutant and relationship between dose and response. Some countries, such as USA, Canada and Australia, regard both respiratory rate and physical activity pattern as main exposure factors for adolescents in both air pollution health risk assessment and exercise risk assessment to forecast a safe exposing condition of pollutant for adolescents while they are doing exercise outdoors. In addition, it suggests that the testing indexes and testing methods of these two exposure factors, such as investigating the time of daily physical activity, strength, and characteristic of frequency, help to set up the quantitative relationship between environmental pollution index and the time, strength, frequency of daily activities, and formulate children's and adolescents' activity instructions under different levels of environmental pollutions. As smog becomes increasingly serious at present, it is meaningful to take physical activity as a critical composition of exposure factor and establish physical activity guideline, so as to reduce the risk of air pollution, and promote physical health of children and adolescents effectively.