Hyponatraemia in patients with cirrhosis.
Hyponatraemia in patients with cirrhosis.
复制标题
肝硬化患者的低钠血症。
DOI：
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发表时间：
1990
期刊：
影响因子：
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通讯作者：
A. Arieff
中科院分区：
文献类型：
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作者：
M. Papadakis;C. L. Fraser;A. Arieff
近一半的肝硬化和腹水住院患者出现低钠血症，这是由于肾脏不能正常排出游离水而导致的过量潴留。低钠血症的发病率和死亡率主要归因于中枢神经系统紊乱。脑含水量增加的程度取决于低钠血症的持续时间和代偿机制。肝硬化患者类固醇和肽激素的改变可能导致低钠血症性脑病的发展，其症状与肝性脑病和尿毒症重叠。脑桥中央髓鞘溶解的发生与低钠血症的矫正率无关。肝硬化患者低钠血症的出现，长期以来被认为是预后不良的迹象，可能是未被识别的潜在肾功能受损的功能。低钠血症的治疗仍不理想。
Hyponatraemia occurs in nearly half of patients in hospital with cirrhosis and ascites, and is due to the excessive retention of free water which results from the kidney's inability to excrete it normally. The morbidity and mortality associated with hyponatraemia is largely attributable to central nervous system disturbances. The degree to which brain water content increases depends on the duration of hyponatraemia and on compensatory mechanisms. Altered steroid and peptide hormones in cirrhotic patients may contribute to the development of hyponatraemic encephalopathy, symptoms of which overlap with hepatic encephalopathy and uraemia. The occurrence of central pontine myelinolysis is unrelated to the rate of correction of hyponatraemia. The appearance of hyponatraemia in cirrhotic patients, long regarded as a poor prognostic sign, may be a function of unrecognized underlying impaired renal function. Therapy for hyponatraemia remains suboptimal.