Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage.

Hypervolemic therapy prevents volume contraction but not hyponatremia following subarachnoid hemorrhage.
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高容量治疗可防止容量收缩,但不能防止蛛网膜下腔出血后出现低钠血症。

DOI:
10.1002/ana.410310513
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发表时间:
1992
影响因子:
11.2
通讯作者:
Hanley,DF
Hanley,DF
中科院分区:
医学1区
文献类型:
--
作者:
Diringer,MN;Wu,KC;Verbalis,JG;Hanley,DF

文献摘要

被引文献

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低钠血症是蛛网膜下腔出血后常见的疾病,也可归因于抗利尿激素分泌不当或钠尿导致血管内容量收缩。我们前瞻性地研究了19名患者的体钠和血管内容量调节,从急性动脉瘤性蛛网膜下腔出血发生后3天开始,以确定高容量治疗对低钠血症和容量收缩的影响,并确定体液因素是否与低钠血症有关。血浆精氨酸加压素、心钠素、肾素活性、醛固酮和儿茶酚胺的系列测定与体内钠和液体平衡、血容量变化、血清钠浓度和渗透压相关。6名患者(32%)出现低钠血症,但只有2名患者出现负钠平衡。在大多数患者中,心钠素水平升高,而血浆肾素活性和醛固酮浓度普遍受到抑制。低钠血症患者血浆精氨酸加压素水平在低渗透压期间不受抑制,且与血清渗透压无关。仅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,但血钠和血浆心钠素水平正常。我们得出的结论是:(1)高容量治疗可防止容量收缩,但不能阻止低钠血症,(2)体液因素可能有利于钠丢失和水分保留,(3)精氨酸加压素调节紊乱,可能导致低钠血症。
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.