［摘要］ 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。

［中图分类号］ R591.1［文献标识码］ A［文章编号］ 1000-1530（2000）04-0369-05

Secondary hyponatremia after Frankel Class-A acute

cervical spinal cord injury

ZHANG Li

(Department of Orthopedics, Peking University Third Hospital, Beijing100083, China)

CAI Qin-Lin

(Department of Orthopedics, Peking University Third Hospital, Beijing100083, China)

DANG Geng-Ding

(Department of Orthopedics, Peking University Third Hospital, Beijing100083, China)

LIU Zhong-Jun

(Department of Orthopedics, Peking University Third Hospital, Beijing100083, China)

ABSTRACTObjective： 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.

KEY WORDSSpinal cord injuries/compl; Hyponatremia/epidemiol; Neck; Hematuria

(J Beijing Med Unvi, 2000,32:369-373)

In recent years, a few reports concerning hyponatremia subsequent spinal cord injury is rare appeared in the literatures. Yet, systematic analysis of its clinical manifestations and regular pattern of pathological charge is still lacking. To our knowledge, there is not any investigation about secondary hyponatremia following acute complete cervical spinal cord injury. The purpose of this study is to clarify the occurrence rate, clinical course, and to discuss the mechanism of secondary hyponatremia after Frankel class-A acute cervical spinal cord injury.

1CLINICAL MATERIALS AND METHODS

Thirty-five patients admitted to the Orthopedic Department of Peking University Third Hospital between 1992 and 1998 were studied. Of these, seven were female and twenty-eight were male, with a mean age of (41 ± 4) years (range 18 to 67 years). All patients suffered from acute cervical spinal cord injury, with a mean interval before admission after injury of (2.8 ± 1.8) days and a mean time of hospitalization of (52 ± 13) days. All the types of spinal cord injury of this group from admission to discharge was Frankel class-A according to Frankel^［1］ classification. All patients had serum electrolyte concentrations determination measurement including sodium, potassium, chlorine, blood urine nitrogen (BUN) and carbon dioxide combining power (CO₂CP). Table 1 shows the intermittent time of serum electrolyte concentrations measurement. Twenty-four hours urine was collected in 18 patients, and the total amount of urinary electrolytes excretion in urine, including sodium, potassium and chlorine were determined in 14.

Table 1The interval of surum electrolytes determination

Week 1st 2nd 3rd - 4th 5th to discharge Average Mean frequency， f/week^－1 2.57 1.86 1.77 1.12 1.35 Intermittent time， t/d 2.72 3.77 7.90 7.79 5.18

All data were analyzed with Microsoft Excel 97 software. Data show with ±s.

2RESULTS

Transient or sustained hyponatremia occurred in all patients in the hospitalized period and the occurrence of hyponatremia in the group was 100%. After hyponatremia, all patients were given 2% - 3% hyperosmotic sodium solution regularly, 30g to 60g each day. The hyponatremia in 15 cases was incorrigible although the degree of hyponatremia abated during hospitalization. Hyponatremia, when it occurred, developed (4.5±1.2) days postinjury, reached its nadir at (14±3) days and began to recover at (39±10) days. Table 2 demonstrates the mean duration of various degree of hyponatremia.

Table 2The mean duration time of every degree

of hyponatremia in 35 patients(±s)

c(Na^＋）/mmol^．L^－1 t/d ～135 20.8 ±6.6 ～130 8.2 ±3.2 ～125 3.8 ±2.9 ～120 1.3 ±1.3 ～115 0.2 ±0.3 ～110 0.1 ±0.1 ～105 0.0 ±0.0 ～100 0.1 ±0.1

t, Mean duration time.Figures 1-3 show the trends of the records of relative serum electrolyte concentrations of thirty-five patients. Besides hyponatremia, there ware hypercapnia and hypernitremia within 30 days after injury in the group. Serum potassium and chlorine always fluctuated within the normal value ranges.

Figure 1(left) The trend of the change of serum sodium after cervical spinal cord injury in 35 cases. The abscissa presents the day of postinjury. The normal value of serum sodium is 135-145 mmol^．L^－1. The mean serum sodium values were lower than normal value from about 4.49 days postinjury in 35 cases.

Figure 2(right) The trend of the records of serum carbon dioxide combining power (CO₂CP) after cervical spinal cord injury in 35 cases. The abscissa presents the day of postinjury. The normal value of serum CO₂CP is 25-32 mmol^．L^－1. The mean serum CO₂CP values of patients were always below the normal value ranges.

Figure 3(left) The trend of the records of blood urine nit