Siegel Arthur J
Internal Medicine, McLean Hospital, Belmont, Massachusetts 02478, USA.
Sports Med. 2007;37(4-5):459-62. doi: 10.2165/00007256-200737040-00049.
Exercise-associated hyponatraemia (EAH) is an acute-onset imbalance in the tonicity of extracellular fluids during or after endurance exercise which results in a blood sodium concentration <135 mmol/L. Both excessive fluid intake and a concurrent decrease in urine formation contribute to this rapid-onset, predominantly dilutional, decrease in serum sodium, which can result in life-threatening pulmonary and cerebral oedema. Marathon runners with hypotonic encephalopathy related to EAH, including two cases with fatal cerebral oedema, demonstrated non-osmotic secretion of arginine vasopressin and fulfilled the essential diagnostic criteria for the syndrome of inappropriate antidiuretic hormone secretion (SIADH). The pathophysiology of SIADH as the proximate cause of EAH accounts for otherwise puzzling clinical observations such as cases occurring after only moderate fluid intake or presenting hours after races. This formulation provides a framework for enhancing prevention by monitoring weight changes during races to detect positive fluid balance before the onset of mental status changes. Most importantly, SIADH supports a strategy for use of oral and intravenous hypertonic solutions, including 3% sodium chloride, for the emergent treatment of moderate and life-threatening symptoms of hypotonic encephalopathy, respectively.
运动相关性低钠血症（EAH）是耐力运动期间或之后细胞外液张力的急性失衡，导致血钠浓度<135 mmol/L。过量液体摄入和同时尿量减少共同导致血清钠迅速下降，主要为稀释性下降，这可能导致危及生命的肺水肿和脑水肿。患有与EAH相关的低渗性脑病的马拉松运动员，包括两例致命性脑水肿患者，表现出精氨酸加压素的非渗透性分泌，并符合抗利尿激素分泌不当综合征（SIADH）的基本诊断标准。SIADH作为EAH的直接病因的病理生理学解释了一些令人困惑的临床观察结果，例如仅在适度液体摄入后发生或在比赛数小时后出现的病例。这一表述为通过在比赛期间监测体重变化以在精神状态改变之前检测到正液体平衡来加强预防提供了一个框架。最重要的是，SIADH支持分别使用口服和静脉高渗溶液（包括3%氯化钠）来紧急治疗低渗性脑病的中度和危及生命症状的策略。
