Department of Medical and Surgical Sciences, Alma Mater Studiorum, University of Bologna, Policlinico S. Orsola-Malpighi, Via Albertoni, 15, 40138, Bologna, Italy.
Hepatol Int. 2018 Nov;12(6):487-499. doi: 10.1007/s12072-018-9894-6. Epub 2018 Sep 10.
Hypervolemic (dilutional) hyponatremia is the most common dysnatremia in cirrhosis, with a prevalence close to 50% in patients with ascites, while hypovolemic hyponatremia occurs in a minority of cases. Hyponatremia carries a poor prognosis, being associated with increased mortality and reduced survival after liver transplantation. Hypernatremia is rarer and is also associated with an adverse prognosis. Increased non-osmotic secretion of arginine vasopressin and altered renal tubular sodium handling due to impaired free water generation are the mechanisms leading to hypervolemic hyponatremia, while diuretic-induced fluid loss is the main cause of hypovolemic hyponatremia. Hypernatremia usually follows hypotonic fluid losses due to osmotic diuresis (glycosuria) or lactulose-induced diarrhea. The main clinical manifestations of dysnatremias are due to their effects on the central nervous system: astroglial cell hyperhydration follows hyponatremia-an abnormality that exacerbates ammonia neurotoxicity-while the opposite abnormality occurs with hypernatremia. Asymptomatic or mildly symptomatic hypervolemic hyponatremia is mainly managed by correcting of precipitating factors and non-osmotic fluid restriction. Severe, life-threatening hyponatremia requires hypertonic saline infusion, avoiding rapid and complete correction of serum sodium concentration to prevent neurological sequelae such as osmotic demyelination. V receptor blockade by vaptans may be considered in patients with sustained hyponatremia waitlisted for liver transplantation. Diuretic withdrawal and plasma volume expansion are required in hypovolemic hypernatremia. Prompt recognition, removal of the precipitating factor(s) and non-osmotic fluid administration represent the mainstays of hypernatremia management. Rapid correction of long-standing hypernatremia can lead to cerebral edema and has to be avoided.
高容量（稀释性）低钠血症是肝硬化中最常见的电解质紊乱，腹水患者中其患病率接近 50%，而低容量性低钠血症则较少见。低钠血症预后不良，与肝移植后死亡率增加和生存率降低有关。高钠血症较罕见，也与不良预后相关。由于自由水生成受损导致抗利尿激素非渗透性分泌增加和肾小管钠处理改变，是导致高容量性低钠血症的机制，而利尿剂引起的液体丢失是低容量性低钠血症的主要原因。高钠血症通常继发于低渗性液体丢失，如渗透性利尿（糖尿）或乳果糖诱导的腹泻。电解质紊乱的主要临床表现是由于其对中枢神经系统的影响：低钠血症引起星形胶质细胞过度水合——这一异常会加重氨的神经毒性——而高钠血症则会出现相反的异常。无症状或轻度症状性高容量性低钠血症主要通过纠正诱发因素和非渗透性液体限制来治疗。严重的、危及生命的低钠血症需要输注高渗盐水，避免过快和完全纠正血清钠浓度，以防止渗透性脱髓鞘等神经后遗症。对于等待肝移植的持续性低钠血症患者，可考虑使用 V 型受体阻滞剂。低容量性高钠血症需要停用利尿剂和扩容。快速识别、去除诱发因素和给予非渗透性液体是治疗高钠血症的主要方法。长期高钠血症的快速纠正可能导致脑水肿，必须避免。
