Frankel-A型急性颈脊髓损伤后继发的低钠血症

目的:总结急性完全性颈脊髓损伤继发低钠血症的发生率及变化规律,并推测其发生机制.方法: 回顾总结分析了本院1992～1998年住院的35例急性Frankel-A型颈脊髓损伤患者的血尿生化变化及其时间变化规律.结果:35例急性颈脊髓损伤患者伤后平均(2.8±1.8) d入院,平均住院时间(52±13) d.低钠血症发生率100%,低钠血症于伤后(4.5±1.2) d开始,(14±3) d达高峰,15例(42.88%)出院时低钠血症仍未恢复.此外,还可出现高碳酸血症、氮质血症、多尿以及尿钠排出量明显增多等变化,而血钾的变化始终在正常范围内波动. 结论: 严重、顽固的低钠血症是颈脊髓损伤后极为常见的并发症,其发生机制可能与脑耗盐综合征有关.

Secondary hyponatremia after Frankel Class-A acute cervical spinal cord injury

Objective To define the occurrence rate, time course, and potential mechanism of hyponatremia in patients after Frankel Class-A acute cervical spinal cord injury. Methods Analysis of data obtained from a retrospective review of blood and urine records of 35 hospitalized cases from 1992 to 1998. Results Patients were admitted after (2.8±1.8) days postinjury and had been hospitalized for (52±13) days. Hyponatremia, the occurrence rate of which was 100%, developed at a mean time of (4.5±1.2) days postinjury, reached its nadir at the end of (14±3) days and recovered to normal at (39±10) days. Fifteen (42.88%) cases did not recover from hyponatremia in the hospitalized period. Patients were suffering from hypercapnia, hypernitremia, polyuria, and hyper-natriuresis besides kalemia. Conclusion Severe and obstinate hyponatremia is a very common complication of cervical spinal cord injury. The mechanism may be related to the Cerebral Salt Wasting Syndrome.