Objective;To investigate etiologic factors,mechanisms and treatment of hyponatremia in patients with acute spinal cord injury. Methods: From January 2005 to July 2010,57 patients with hyponatremia after acute spinal cord injuries from severe trauma were treated. They included 46 males and 11 females who ranged in age from 26 to 69 years (mean 39.5 years). Of the 57 cases,55 cases were complicated by cervical dislocation or fracture,and the remaining two cases were without dislocation or fracture. Among them, 28 patients had complete spinal cord injury, 29 had incomplete spinal cord injury. Nerve function was assessed according to the ASIA criteria,revealing type A in 28 cases,type B in 25 cases,and type C in 4 cases. Heart rate, blood pressure,24-hour urine volume and serum sodium were measured daily,and fluid and sodium replacement was administered when the diagnosis of hyponatremia was confirmed. Urine sodium,serum osmotic pressure and urine osmotic pressure were measured every 3 days. The potential cause of the hyponatremia was supposed to be cerehral salt wasting syndrome (CSWS) or inappropriate antidiuretic hormone secretion (SIADH) according to the results and therapeutic reaction. Intravenous fluid infusion and salt replacement were required in patients with CSWS,while fluid restriction and intravenous salt replacement were administered for patients with SIADH. Parameters before and after treatment were analyzed with t-test. Rfi-SultS;There were 42 patients with SCWS.and 15 patients with SIADH. Heart rate,serum sodium and serum osmotic pressure were higher 3 weeks after admission in all patients (all P<0.01),while blood pressure and urine osmotic pressure were higher and urine sodium was lower (all ZMX05). There was no significant difference in 24-h urine volume (P>0.05). Heart rate, serum osmotic pressure, urine osmotic pressure showed further improvement by the time of discharge, while 24—h urine volume decreased, urine sodium further decreased (all P<0.05). There was no significant change in blow) pressure (P>0.05). Conclusion: CSWS and SIADH are two potential causes of hyponatremia in patients with acute spinal cord injury. Distinguishing between these two disorders is of crucial importance because treatment of each condition is quite different, one needing vigorous salt replacement while the other needing fluid restriction.%目的:探讨急性颈脊髓损伤患者并发低钠血症的病因、发病机制和治疗方法.方法:自2005年1月至2010年7月收治严重创伤导致急性颈脊髓损伤伴高位截瘫并发低钠血症患者57例,男46例,女11例;年龄26～69岁,平均39.5岁；颈椎骨折或脱位55例,无骨折或脱位型脊髓损伤2例；完全性损伤28例,不完全性损伤29例.神经功能损害按ASIA分级:A级28例,B级 25例,C级4例.每日监测心率、血压、尿量、血钠,诊断低钠血症后即开始静脉补液、补钠,每隔2d检测尿钠、血浆渗透压、尿渗透压,根据监测结果及治疗反应判断低钠原因是由脑性盐耗综合征(CSWS)还是由抗利尿激素不适当分泌综合征(SIADH)引起,前者继续静脉补液、补钠,后者严格限水同时静脉补钠直至低钠纠正.对治疗前后血钠等指标进行统计学分析.结果:57例中诊断CSWS者42例,SIADH者15例.治疗3周后所有患者的心率、血钠、血渗透压有明显回升(P＜0.01),血压、尿渗透压升高,尿钠减少(均P＜0.05),尿量未见明显减少(P＞0.05).出院时与治疗3周比较,心率、血浆渗透压、尿渗透压进一步回升,尿量减少,尿钠进一步减少(P＜0.05),血压无明显改变(P＞0.05).结论:急性颈脊髓损伤后并发低钠血症受多因素影响,发病机制主要为脑性盐耗综合征(SCWS)及抗利尿激素不适当分泌综合征(SIADH),治疗时应注意鉴别,根据不同病因采取补液或限液治疗.
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