Misra Usha K, Kalita Jayantee
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
Wellcome Open Res. 2021 Mar 29;4:189. doi: 10.12688/wellcomeopenres.15502.2. eCollection 2019.
Hyponatremia is the commonest electrolyte abnormality in hospitalized patients and is associated with poor outcome. Hyponatremia is categorized on the basis of serum sodium into severe (< 120 mEq/L), moderate (120-129 mEq/L) and mild (130-134mEq/L) groups. Serum sodium has an important role in maintaining serum osmolality, which is maintained by the action of antidiuretic hormone (ADH) secreted from the posterior pituitary, and natriuretic peptides such as atrial natriuretic peptide and brain natriuretic peptide. These peptides act on kidney tubules via the renin angiotensin aldosterone system. Hyponatremia <120mEq/L or a rapid decline in serum sodium can result in neurological manifestations, ranging from confusion to coma and seizure. Cerebral salt wasting (CSW) and syndrome of inappropriate secretion of ADH (SIADH) are important causes of hyponatremia in tuberculosis meningitis (TBM). CSW is more common than SIADH. The differentiation between CSW and SIADH is important because treatment of one may be detrimental for the other; evidence of hypovolemia in CSW and euvolemia or hypervolemia in SIADH is used for differentiation. In addition, evidence of dehydration, polyuria, negative fluid balance as assessed by intake output chart, weight loss, laboratory evidence and sometimes central venous pressure are helpful in the diagnosis of these disorders. Volume contraction in CSW may be more protracted than hyponatremia and may contribute to border zone infarctions in TBM. Hyponatremia should be promptly and carefully treated by saline and oral salt, while 3% saline should be used in severe hyponatremia with coma and seizure. In refractory patients with hyponatremia, fludrocortisone helps in early normalization of serum sodium without affecting polyuria or functional outcome. In SIADH, V2 receptor antagonist conivaptan or tolvaptan may be used if the patient is not responding to fluid restriction. Fluid restriction in SIADH has not been found to be beneficial in TBM and should be avoided.
低钠血症是住院患者中最常见的电解质异常，且与不良预后相关。低钠血症根据血清钠水平分为重度（<120 mEq/L）、中度（120 - 129 mEq/L）和轻度（130 - 134 mEq/L）组。血清钠在维持血清渗透压方面起重要作用，血清渗透压由垂体后叶分泌的抗利尿激素（ADH）以及心房利钠肽和脑利钠肽等利钠肽的作用来维持。这些肽通过肾素 - 血管紧张素 - 醛固酮系统作用于肾小管。血清钠<120 mEq/L或血清钠快速下降可导致神经学表现，从意识模糊到昏迷和癫痫发作。脑性盐耗综合征（CSW）和抗利尿激素分泌不当综合征（SIADH）是结核性脑膜炎（TBM）中低钠血症的重要原因。CSW比SIADH更常见。区分CSW和SIADH很重要，因为对其中一种的治疗可能对另一种有害；CSW中的血容量减少证据以及SIADH中的血容量正常或血容量过多证据用于区分。此外，脱水、多尿、根据出入量图表评估的负液体平衡、体重减轻、实验室证据以及有时中心静脉压等证据有助于诊断这些疾病。CSW中的容量收缩可能比低钠血症更持久，并且可能导致TBM中的边缘带梗死。低钠血症应通过生理盐水和口服盐迅速且谨慎地治疗，而对于伴有昏迷和癫痫发作的重度低钠血症应使用3%生理盐水。对于难治性低钠血症患者，氟氢可的松有助于血清钠早期恢复正常，而不影响多尿或功能结局。在SIADH中，如果患者对液体限制无反应，可使用V2受体拮抗剂考尼伐坦或托伐普坦。在TBM中，尚未发现SIADH中的液体限制有益，应避免使用。
