小脑幕切迹疝后高钠血症的临床分析

目的探讨小脑幕切迹疝与高钠血症的关系,及其病因、发生机制、对患者预后的影响及防治对策。方法回顾性分析116例脑科手术患者资料,结合患者的发病机制、颅脑损伤部位、发病后的治疗方案,探求小脑幕切迹疝后发生高钠血症的病因。总结患者的临床资料和临床转归,并对所得结果进行统计学分析。结果高钠血症与脑疝、脑损伤的严重程度、脱水剂的应用、24h液体出入量关系密切,并发高钠血症的脑科患者病死率明显增高。68例脑疝组,其中,高钠血症45例,无高钠血症23例,非脑疝组48例,高钠血症6例,无高钠血症42例,较脑疝组脑疝组较无脑疝组,其高钠血症发生率相对升高。60例术后脑疝解除者,其中,高钠血症39例,术后脑疝未解除的14例中,高钠血症6例。116例患者死亡79例,其中高钠血症26例,无高钠血症53例,二者比较差异有统计学意义。结论医源性脱水过度及下丘脑损害致水电解质失衡是高钠血症的主要原因,尽快解除脑疝、治疗原发病、密切监测血钠浓度、及时调整水电解质平衡、是防治脑科患者术后高钠血症的关键。

The clinical analysis of hypernatronemia after transtentorial herniation

Objective To explore the relationship between transtentorial herniation （TH） and hypernatronemia, its eti- ology, pathogenesis, impact on prognosis, and countermeasures. Methods Data of 116 patients with brain surgery were retrospectively analyzed to detect whether hypernatronemia occurred or not after surgery. Combining with each patient＇s pathogenesis, location of craniocerebral injury, and treatment strategy, the causes of hypernatronemia after TH were discussed. All possibilities were statistically analyzed based on summarizations of clinical data and outcomes. Results The hypernatronemia was closely related with cerebral hernia, severity of cerebral injury, application of dehydrant, and liquid output and intake in 24 hours. The fatality rate of cerebral injury patients with hypernatronemia was obviously increased. To be specific, in cerebral hernia group （n=68）, the number of patients with hypernatronemia was 45, while in non-cerebral hernia group （n=48）, the proportion of patients suffered from hypernatronemia was 12.5%. Compared with non-cerebral hernia group, incidence of hypernatronemia in the cerebral group was relatively higher. Among 60 patients removing cerebral hernia, there were 39 cases suffering from hypernatronemia. While for 14 cases failing to remove cerebral hernia, 6 patients with hypernatronemia occurred. There were 79 patients dead among all participants, from which 26 patients suffered from hypernatronemia with a statistical difference in comparison of the two groups. Conclusion Iatrogenic excessive dehydration and imbalance of water-electrolyte due to hypothalamus damage were the principal causes for hypernatronemia. The key factors to prevent and treat cerebral injury patients with hypernatrone- mia after operation were removing cerebral hernia, focusing on protopathy, close monitoring on serum sodium concen- tration and timely adjusting water-electrolyte balance.