Diringer M N, Wu K C, Verbalis J G, Hanley D F
Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, MD.
Ann Neurol. 1992 May;31(5):543-50. doi: 10.1002/ana.410310513.
Hyponatremia is common following subarachnoid hemorrhage and has alternatively been attributed to either the inappropriate secretion of antidiuretic hormone or natriuresis causing intravascular volume contraction. We prospectively studied body sodium and intravascular volume regulation in 19 patients, beginning within 3 days after acute aneurysmal subarachnoid hemorrhage occurred, in order to determine the impact of hypervolemic therapy on both hyponatremia and volume contraction and to ascertain whether humoral factors account for hyponatremia. Serial measurements of plasma arginine vasopressin, atrial natriuretic factor, renin activity, aldosterone, and catecholamines were correlated with body sodium and fluid balance, change in blood volume, serum sodium concentration, and osmolality. Six patients (32%) developed hyponatremia, but only 2 had a negative sodium balance. In most patients, levels of atrial natriuretic factor were elevated, while plasma renin activity and aldosterone concentrations were generally suppressed. Plasma arginine vasopressin levels were not suppressed during hypo-osmolality and did not correlate with serum osmolality in hyponatremic patients. Only 1 patient had a decrease in blood volume, which was associated with marked rises in aldosterone and plasma renin activity, but normal serum sodium and plasma atrial natriuretic factor levels. We conclude that following subarachnoid hemorrhage: (1) Hypervolemic therapy prevents volume contraction but not hyponatremia, (2) humoral factors may favor both sodium loss and water retention, and (3) arginine vasopressin regulation is disturbed and may contribute to hyponatremia.
低钠血症在蛛网膜下腔出血后很常见，其原因一直被认为要么是抗利尿激素分泌不当，要么是利钠导致血管内容量收缩。我们对19例患者进行了前瞻性研究，在急性动脉瘤性蛛网膜下腔出血发生后的3天内开始研究机体钠和血管内容量调节，以确定高血容量疗法对低钠血症和容量收缩的影响，并确定体液因素是否是低钠血症的原因。对血浆精氨酸加压素、心房利钠因子、肾素活性、醛固酮和儿茶酚胺进行系列测量，并与机体钠和液体平衡、血容量变化、血清钠浓度和渗透压相关联。6例患者（32%）发生了低钠血症，但只有2例钠平衡为负。在大多数患者中，心房利钠因子水平升高，而血浆肾素活性和醛固酮浓度通常受到抑制。低渗状态下血浆精氨酸加压素水平未被抑制，且与低钠血症患者的血清渗透压无关。只有1例患者血容量减少，这与醛固酮和血浆肾素活性显著升高有关，但血清钠和血浆心房利钠因子水平正常。我们得出结论，蛛网膜下腔出血后：（1）高血容量疗法可防止容量收缩，但不能防止低钠血症；（2）体液因素可能有利于钠丢失和水潴留；（3）精氨酸加压素调节受到干扰，可能导致低钠血症。
