Department of Medicine, University of Florida College of Medicine, Jacksonville, FL 32209, USA.
Int J Clin Pract. 2009 Oct;63(10):1494-508. doi: 10.1111/j.1742-1241.2009.02103.x.
Hyponatraemia is a commonly encountered electrolyte abnormality in hospitalised patients and is associated with significant morbidity and mortality. The fact that most cases of hyponatraemia are the result of water imbalance rather than sodium imbalance underscores the role of antidiuretic hormone (ADH) in the pathophysiology. Hyponatraemia can be classified according to the measured plasma osmolality as isotonic, hypertonic or hypotonic. Hyponatraemia with a normal plasma osmolality usually indicates pseudohyponatraemia, while hyponatraemia because of a high plasma osmolality is typically caused by hyperglycaemia. After excluding isotonic and hypertonic causes, hypotonic hyponatraemia is further classified according to the volume status of the patient as hypovolaemic, hypervolaemic or euvolaemic. Hypovolaemic hyponatraemia is accompanied by extracellular fluid (ECF) volume deficit, while hypervolaemic hyponatraemia manifests with ECF volume expansion. The syndrome of inappropriate ADH (SIADH) should be suspected in any patient with euvolaemic hyponatraemia with a urine osmolality above 100 mOsm/kg and urine sodium concentration above 40 mEq/l. In the management of any hyponatraemia regardless of the patient's volume status, it is advised to restrict free water and hypotonic fluid intake. Hypertonic saline and vasopressin antagonists can be used to correct symptomatic hyponatraemia. The rate of correction is dependent upon the duration, degree of hyponatraemia and the presence or absence of symptoms. Symptomatic acute hyponatraemia (< 48 h) is a medical emergency requiring rapid correction to prevent the worsening of brain oedema. In asymptomatic patients with chronic hyponatraemia (> 48 h or unknown duration), fluid restriction and close monitoring alone are sufficient, while a slow correction by 0.5 mEq/l/h may be attempted in symptomatic patients. Excessive rapid correction should be avoided in both acute and chronic hyponatraemia, because it can lead to irreversible neurological complications including central osmotic demyelination.
低钠血症是住院患者中常见的电解质异常，与显著的发病率和死亡率相关。事实上，大多数低钠血症病例是由于水失衡而不是钠失衡引起的，这突出了抗利尿激素（ADH）在病理生理学中的作用。根据测量的血浆渗透压，低钠血症可分为等渗性、高渗性或低渗性。等渗性低钠血症通常提示假性低钠血症，而高渗性低钠血症通常由高血糖引起。排除等渗性和高渗性原因后，根据患者的容量状态进一步将低渗性低钠血症分为低血容量、高血容量或血容量正常。低血容量性低钠血症伴有细胞外液（ECF）容量不足，而高血容量性低钠血症表现为 ECF 容量扩张。对于任何血容量正常的低钠血症患者，如果尿渗透压大于 100 mOsm/kg 且尿钠浓度大于 40 mEq/l，则应怀疑为抗利尿激素不适当分泌综合征（SIADH）。无论患者的容量状态如何，在治疗任何低钠血症时，建议限制自由水和低渗液的摄入。高渗盐水和血管加压素拮抗剂可用于纠正有症状的低钠血症。纠正速度取决于低钠血症的持续时间、严重程度以及是否存在症状。有症状的急性低钠血症（<48 h）是一种医疗紧急情况，需要迅速纠正以防止脑水肿恶化。对于无症状的慢性低钠血症患者（>48 h 或未知持续时间），单独限制液体摄入和密切监测即可，而对于有症状的患者，可尝试以 0.5 mEq/l/h 的速度缓慢纠正。无论是急性还是慢性低钠血症，都应避免过度快速纠正，因为这可能导致不可逆的神经并发症，包括中心渗透压脱髓鞘。
