Wang He, Hu Yong
The Intensive Care Unit of Ningbo No. 6 Hospital, Ningbo 315040, Zhejiang, China.
Zhongguo Gu Shang. 2012 Apr;25(4):306-9.
To investigate etiologic factors,mechanisms and treatment of hyponatremia in patients with acute spinal cord injury.
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 cerebral 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.
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 P < 0.05). 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 blood pressure (P > 0.05).
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.
探讨急性脊髓损伤患者低钠血症的病因、机制及治疗方法。
选取2005年1月至2010年7月间57例因严重创伤导致急性脊髓损伤后出现低钠血症的患者。其中男性46例,女性11例,年龄26至69岁(平均39.5岁)。57例患者中,55例合并颈椎脱位或骨折,其余2例无脱位或骨折。其中,28例为完全性脊髓损伤,29例为不完全性脊髓损伤。根据美国脊髓损伤协会(ASIA)标准评估神经功能,结果显示A级28例,B级25例,C级4例。每日测量心率、血压、24小时尿量及血清钠,确诊低钠血症后给予补液及补钠治疗。每3天测量尿钠、血清渗透压及尿渗透压。根据结果及治疗反应推测低钠血症的可能病因是脑性盐耗综合征(CSWS)或抗利尿激素分泌不当综合征(SIADH)。CSWS患者需静脉补液及补盐,SIADH患者则需限制液体摄入并静脉补盐。治疗前后参数采用t检验进行分析。
42例为CSWS,15例为SIADH。所有患者入院3周后心率、血清钠及血清渗透压均升高(均P<0.01),而血压及尿渗透压升高,尿钠降低(均P<0.05)。24小时尿量差异无统计学意义(P>0.05)。出院时心率、血清渗透压、尿渗透压进一步改善,而24小时尿量减少,尿钠进一步降低(均P<0.05)。血压无明显变化(P>0.05)。
CSWS和SIADH是急性脊髓损伤患者低钠血症的两个潜在病因。区分这两种疾病至关重要,因为每种疾病的治疗方法截然不同,一种需要积极补盐,而另一种需要限制液体摄入。