Frankel-A型急性颈脊髓损伤后继发的低钠血症
作者：张立 蔡钦林 党耕町 刘忠军
单位：北京大学第三医院骨科，北京 100083
关键词：脊髓损伤；并发症；低钠血症；流行病学；颈；血尿
北京医科大学学报000425 [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。
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[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, Beijing 100083, China)
CAI Qin-Lin
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
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DANG Geng-Ding
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
LIU Zhong-Jun
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
ABSTRACT 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.
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KEY WORDS Spinal 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.
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1 CLINICAL 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.
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Table 1 The 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
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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.
2 RESULTS
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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, 30 g to 60 g 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.
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Table 2 The 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
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～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.
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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.
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Figure 3 (left) The trend of the records of blood urine nitrogen (BUN) after cervical spinal cord injury in 35 cases. The abscissa presents the day of postinjury. The normal value of BUN is 2.9-6.0 mmol.L-1. The mean BUN values of patients were higher than normal value within the first 30 days postinjury, and fluctuated within the normal value ranges afterwards.
Figure 4 (right) Twenty-four hours urine volumes, which were recorded in 18 patients, The abscissa presents the day of postinjury. The mean of which were (4 088 ± 169) ml each day and the largest were 8800 ml each day, much more than those in normal (1000-2000 ml each day) with high significance of difference (t test between sample mean and population mean, t=30.55, P<0.01).
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Twenty-four hours urine volumes, which were recorded in 18 patients, mean of those were obviously more than those in normal with high significance of difference (t test between sample mean and population mean, t=30.55, P<0.01， Figure 4).
Twenty-four hours urinary electrolytes excretion amount including sodium, potassium and chlorine were determined in 14 patients with hyponatremia. Figure 5 demonstrates the results. The concentration of sodium in urine was (94±23) mmol.L-1. The twenty-four hours excretion amount of sodium and chlorine in urine were higher than those of the normal with high significance of difference (t test between sample mean and population mean, t value were 4.23 and 3.70 respectively, P<0.01). However, there were no significance of difference (t test between sample mean and population mean, t=1.66, P>0.05) between those of potassium in urine of the normal and of the patients.
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Figure 5 Twenty-four hours sodium [(37±82) mmol.L-1],potassium [(96±23) mmol.L-1] and chlorine [(379±89) mmol.L-1]
excretion volumes in urine after hyponatremia in 14 patients compared
with the normal values respectively.
Three patients in this group died in the hospital. Of whom, two were male and one female. The mean age of them was 63.67 years. The mean time before admission after their injuries was 1.33 days, the hyponatremia developed 2.67 days averagely and reached their nadirs at 11 days averagely and the mean value of serum sodium was 128.61 mmol.L-1 in the hospitalized period. They were dead at a mean time of 11 days after admission.
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3 DICUSSION
It is uncommon to find electrolyte abnormalities in hospitalized patients. In the medical and surgical patient population, and the incidence of hyponatremia has been reported to be 1% and 2.5%, respectively. Recently, there have been a few reports in literatures, that hyponatremia is a common complication after cervical spinal cord injury, reporting that the incidences of the secondary hyponatremia after cervical spinal cord injury were 45% to 77.8%[2-5]. Nevertheless, the above-mentioned literatures had not analyzed the prevalence of secondary hyponatremia after different classification of cervical spinal cord injury. Additionally, there is not any report about the occurrence rate and trends of secondary hyponatremia Frankel Class-A complete cervical spinal cord injury. Our study excluded the possibility that the classification of cervical spinal cord injury interferes the incidence of hyponatremia. The occurrence rate of hyponatremia in our presented group, all cases of which were Frankel Class-A cervical spinal cord injury, was 100%.
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Some literatures reported that the hyponatremia occurred 6.4 to 8.9 days post cervical spinal cord injury and reached its nadir at 8.7 to 12.9 days post injury[3-5]. However, all the mentioned literature either includes too few cases, or confuses the interference of different classifications of cervical spinal cord injury.
Our present acute cervical spinal cord injury cases were admitted at the mean time of (2.8 ± 1.8) days post injury; discharged at the mean time of (52 ± 13) days post admission; got the serum electrolyte examination every 5.18 days (every 2.72 days for the first week and every 3.77 days for the second week after admission respectively). Therefore, our present study could well demonstrate the serum electrolytes trends after acute cervical spinal cord injury. In our investigation, hyponatremia developed (4.5 ± 1) days post injury, reached its nadir (14 ± 3) days post injury and began to recover (39 ± 10) days post injury. Physicians should pay sufficient attention to the hyponatremia, particularly to the acute and severe hyponatremia, which may result in cerebral edema and ischaemia even cerebral herniation and death.
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The results of our investigation show that severe and obstinate hyponatremia is an extremely common complication of cervical spinal cord injury, particularly of the Frankel Class-A. In our present cases, patients got the continuous intravenous administration of hypertonic NaCl solution after hyponatremia. Meanwhile, hyponatremia persisted for a long time of (34 ± 10) days, the longest time of 147 days, and hyponatremia did not recover to normal in the hospitalized period in 15 cases (42.88%). Furthermore, patients were suffering from hypercapnia, hypernitremia, polyuria, and hyper-natriuresis at the time of hyponatremia; and the trends of those tallied with the trends of hypona-tremia; however, the serumpotassium concentration always fluctuated within the normal value ranges.
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Presently, there were many literatures about secondary hyponatremia in neurosurgical patients; nevertheless, the mechanism, which has not been clear, is illustrated with two different theories: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt- wasting syndrome (CSWS). In spite of that, there has not been any report about the study of mechanism of secondary hyponatremia of cervical spinal cord injury.
SIADH, which causes hypervolaemic hyponatremia, could mostly be observed in severe central nervous system disorders. That may be attributed to antidiuretic hormone (ADH) inappropriate secretion increase without the regulation of plasma osmotic pressure or by direct stimulation of the hypothalamus. However, CSWS, which causes renal salt wasting by the impairment of sodium in the renal tubules, may be attributed to the renal nerve inhibition caused by central nervous system disorders[6]. Nevertheless, the basic clinical manifestations of the two syndromes are hyponatremia, plasma hypotonicity and the relative central nervous symptoms caused by hyponatremia. The main differences of the two syndromes are the changing of blood volume and sodium metabolic balance: In SIADH patients, blood volume increase and neutral or positive sodium metabolic balance are seen; in CSWS patients, blood volume decrease, negative sodium metabolic balance or hyper-natriuresis, polyuria and hypernitremia are seen[7].
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The two metabolisms of the two syndromes are different, then the treatments are different. To SIADH, the main management is water restriction, and others including administrations with hypertonic sodium[8]， solution, furosemide, ledermycin and carbamide[8]; to CSWS, the main treatments are administration with normo- or hyper-tonic sodium solution and corticosterone such as fludrocortisone, yet excessive restriction of water may worsen the symptom or even result in death[7，9].
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Though there is not any systematic study about the mechanism of secondary hyponatremia of cervical spinal cord injury, some authors presumed that might be SIADH or autonomic nervous system disturbance according to their clinical surveys[10]. The results of our investigation show that hyponatremia, polyuria, hyper-natriuresis, besides normo-kalemia are common in the patients with cervical spinal cord injury. All these accord with the manifestations of CSWS even more. We assume that sympathetic nerve system may be inhibited after cervical spinal cord injury[11], then renal diuresis and renal salt wasting occur without the control of renal sympathetic nerve. Additionally, that is also a disturbance of autonomic nervous system after cervical spinal cord injury. Our suggestion needs confirmation with further studies.
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Notwithstanding the mechanism has not been clear. Most authors suggest that the main treatments should be administration with 0.513 mol.L-1 hypertonic NaCl solution and water restriction[5]. Unfortunately, the hyponatremia did not be corrected effectively in spite we administrated the patients with intravenous hypertonic NaCl solution 30 to 60 g per day.
Of the three dead cases, the mean age (63.67 years) was higher than that of this group (41 years). Additionally, the mean developed time (2.67 days) and the mean time of reaching the nadir (11 days) of hyponatremia of the three dead cases were earlier than those (4.49 and 13.61 days) of this group respectively. Furthermore, the mean serum sodium (128.61 mmol.L-1) was less than that of this group (131.43 mmol.L-1). We assume that age, the velocity and degree of hyponatremia development are part of the reason for the death of the hyponatremic patients. Yet it is incapable of making clear the relationship between the patient's age and the development of hyponatremia, because the observed cases were not enough.
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The patients we studied were administrated with intravenous mannitol 2 to 3 weeks and intravenous dexamethasone 5 days. In spite of the fact, that mannitol could increase the excretion of water and electrolytes, and the reabsorption of sodium exceeded that of water. Therefore, mannitol could prevent the rat from acute hyponatremia[12]. It is known that corticosteroid has a mild effect of water and sodium retention. Accordingly, the administration with mannitol and corticosteroid to the patients we studied could not promote the development of hyponatremia.
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(Edited by WANG Lei)
REFERENCES
1，Frankel HL, Hancock DO, Hyslop G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia.I[J]. Paraplegia, 1969，7:179-192
2，Biyani A， Inman CG， el Masry WS. Hyponatraemia after acute spinal injury[J]. Injury， 1993， 24: 671-673
3，Peruzzi WT, Shapiro BA, Meyer PR Jr, et al. Hyponatremia in acute spinal cord injury[J]. Crit Care Med， 1994, 22: 252-258
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4，Zhang Li, Dang GD, Guo ZQ, et al. Cervical spinal cord injury and hyponatremia[J]. Journal of Beijing Medical University(北京医科大学学报)， 1995，27:191-193
5，Zhou GC, Zhao WL, Yuan ZM, et al. Syndrome of inappropriate antidiuratic hormone secretion caused by acute cervical spinal cord injury[J]. Chinese Journal of Spine and Spinal Cord(中国脊柱脊髓杂志)， 1995， 5: 193-196
6，Welt LG, Seldin DW, Nelson WP, et al. Role of the central nervour system in metabolism of electrolytes and water[J]. Arch Int Med, 1952，90:355-378
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7，Wijdicks EF， Vermeulen M， van Brummelen P， et al. Digoxin-like immunoreactive substance in patients with aneurysmal subarachnoid haemorrhage[J]. Br Med J,1987，294:729-732
8，Decaux G, Prospert F, Penninckx R, et al. 5-year treatment of the chronic syndrome of inappropriate secretion of ADH with oral urea[J]. Nephron, 1993，63:468-470
9，Oster JP, Perez GO, Larios O, et al. Cerebral salt wasting in a man with carcinomatous meningitis[J]. Arch Intern Med, 1983，143:2187-2188
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10，Wall BM, Williams HH， Presley DN， et al. Altered sensitivity of osmotically stimulated vasopressin release in quadriplegic subjects[J]. Am J Physiol， 1990，258:R827-35
11，Colachis SC. Autonomic hyperreflexia with spinal cord injury[J]. J Am Paraplegia Soc, 1992，15:3,171-186
12，Gowrishankar M, Chen CB, Cheema-Dhadli S, et al. Prevention of acute hyponatremia by mannitol: an unanticipated mechanism[J]. Clin Nephrol, 1998， 50: 295-300
(Received 2000-03-09), 百拇医药
单位：北京大学第三医院骨科，北京 100083
关键词：脊髓损伤；并发症；低钠血症；流行病学；颈；血尿
北京医科大学学报000425 [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。
, 百拇医药
[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, Beijing 100083, China)
CAI Qin-Lin
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
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DANG Geng-Ding
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
LIU Zhong-Jun
(Department of Orthopedics, Peking University Third Hospital, Beijing 100083, China)
ABSTRACT 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.
, http://www.100md.com
KEY WORDS Spinal 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.
, http://www.100md.com
1 CLINICAL 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.
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Table 1 The 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
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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.2 RESULTS
, 百拇医药
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, 30 g to 60 g 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.
, 百拇医药
Table 2 The mean duration time of every degree
of hyponatremia in 35 patients (
±s) c(Na+)/mmol.L-1t/d
～135
20.8 ±6.6
～130
8.2 ±3.2
～125
3.8 ±2.9
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～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.
, 百拇医药
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.
, 百拇医药
Figure 3 (left) The trend of the records of blood urine nitrogen (BUN) after cervical spinal cord injury in 35 cases. The abscissa presents the day of postinjury. The normal value of BUN is 2.9-6.0 mmol.L-1. The mean BUN values of patients were higher than normal value within the first 30 days postinjury, and fluctuated within the normal value ranges afterwards.
Figure 4 (right) Twenty-four hours urine volumes, which were recorded in 18 patients, The abscissa presents the day of postinjury. The mean of which were (4 088 ± 169) ml each day and the largest were 8800 ml each day, much more than those in normal (1000-2000 ml each day) with high significance of difference (t test between sample mean and population mean, t=30.55, P<0.01).
, 百拇医药
Twenty-four hours urine volumes, which were recorded in 18 patients, mean of those were obviously more than those in normal with high significance of difference (t test between sample mean and population mean, t=30.55, P<0.01， Figure 4).
Twenty-four hours urinary electrolytes excretion amount including sodium, potassium and chlorine were determined in 14 patients with hyponatremia. Figure 5 demonstrates the results. The concentration of sodium in urine was (94±23) mmol.L-1. The twenty-four hours excretion amount of sodium and chlorine in urine were higher than those of the normal with high significance of difference (t test between sample mean and population mean, t value were 4.23 and 3.70 respectively, P<0.01). However, there were no significance of difference (t test between sample mean and population mean, t=1.66, P>0.05) between those of potassium in urine of the normal and of the patients.
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Figure 5 Twenty-four hours sodium [(37±82) mmol.L-1],potassium [(96±23) mmol.L-1] and chlorine [(379±89) mmol.L-1]
excretion volumes in urine after hyponatremia in 14 patients compared
with the normal values respectively.
Three patients in this group died in the hospital. Of whom, two were male and one female. The mean age of them was 63.67 years. The mean time before admission after their injuries was 1.33 days, the hyponatremia developed 2.67 days averagely and reached their nadirs at 11 days averagely and the mean value of serum sodium was 128.61 mmol.L-1 in the hospitalized period. They were dead at a mean time of 11 days after admission.
, http://www.100md.com
3 DICUSSION
It is uncommon to find electrolyte abnormalities in hospitalized patients. In the medical and surgical patient population, and the incidence of hyponatremia has been reported to be 1% and 2.5%, respectively. Recently, there have been a few reports in literatures, that hyponatremia is a common complication after cervical spinal cord injury, reporting that the incidences of the secondary hyponatremia after cervical spinal cord injury were 45% to 77.8%[2-5]. Nevertheless, the above-mentioned literatures had not analyzed the prevalence of secondary hyponatremia after different classification of cervical spinal cord injury. Additionally, there is not any report about the occurrence rate and trends of secondary hyponatremia Frankel Class-A complete cervical spinal cord injury. Our study excluded the possibility that the classification of cervical spinal cord injury interferes the incidence of hyponatremia. The occurrence rate of hyponatremia in our presented group, all cases of which were Frankel Class-A cervical spinal cord injury, was 100%.
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Some literatures reported that the hyponatremia occurred 6.4 to 8.9 days post cervical spinal cord injury and reached its nadir at 8.7 to 12.9 days post injury[3-5]. However, all the mentioned literature either includes too few cases, or confuses the interference of different classifications of cervical spinal cord injury.
Our present acute cervical spinal cord injury cases were admitted at the mean time of (2.8 ± 1.8) days post injury; discharged at the mean time of (52 ± 13) days post admission; got the serum electrolyte examination every 5.18 days (every 2.72 days for the first week and every 3.77 days for the second week after admission respectively). Therefore, our present study could well demonstrate the serum electrolytes trends after acute cervical spinal cord injury. In our investigation, hyponatremia developed (4.5 ± 1) days post injury, reached its nadir (14 ± 3) days post injury and began to recover (39 ± 10) days post injury. Physicians should pay sufficient attention to the hyponatremia, particularly to the acute and severe hyponatremia, which may result in cerebral edema and ischaemia even cerebral herniation and death.
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The results of our investigation show that severe and obstinate hyponatremia is an extremely common complication of cervical spinal cord injury, particularly of the Frankel Class-A. In our present cases, patients got the continuous intravenous administration of hypertonic NaCl solution after hyponatremia. Meanwhile, hyponatremia persisted for a long time of (34 ± 10) days, the longest time of 147 days, and hyponatremia did not recover to normal in the hospitalized period in 15 cases (42.88%). Furthermore, patients were suffering from hypercapnia, hypernitremia, polyuria, and hyper-natriuresis at the time of hyponatremia; and the trends of those tallied with the trends of hypona-tremia; however, the serumpotassium concentration always fluctuated within the normal value ranges.
, 百拇医药
Presently, there were many literatures about secondary hyponatremia in neurosurgical patients; nevertheless, the mechanism, which has not been clear, is illustrated with two different theories: syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and cerebral salt- wasting syndrome (CSWS). In spite of that, there has not been any report about the study of mechanism of secondary hyponatremia of cervical spinal cord injury.
SIADH, which causes hypervolaemic hyponatremia, could mostly be observed in severe central nervous system disorders. That may be attributed to antidiuretic hormone (ADH) inappropriate secretion increase without the regulation of plasma osmotic pressure or by direct stimulation of the hypothalamus. However, CSWS, which causes renal salt wasting by the impairment of sodium in the renal tubules, may be attributed to the renal nerve inhibition caused by central nervous system disorders[6]. Nevertheless, the basic clinical manifestations of the two syndromes are hyponatremia, plasma hypotonicity and the relative central nervous symptoms caused by hyponatremia. The main differences of the two syndromes are the changing of blood volume and sodium metabolic balance: In SIADH patients, blood volume increase and neutral or positive sodium metabolic balance are seen; in CSWS patients, blood volume decrease, negative sodium metabolic balance or hyper-natriuresis, polyuria and hypernitremia are seen[7].
, 百拇医药
The two metabolisms of the two syndromes are different, then the treatments are different. To SIADH, the main management is water restriction, and others including administrations with hypertonic sodium[8]， solution, furosemide, ledermycin and carbamide[8]; to CSWS, the main treatments are administration with normo- or hyper-tonic sodium solution and corticosterone such as fludrocortisone, yet excessive restriction of water may worsen the symptom or even result in death[7，9].
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Though there is not any systematic study about the mechanism of secondary hyponatremia of cervical spinal cord injury, some authors presumed that might be SIADH or autonomic nervous system disturbance according to their clinical surveys[10]. The results of our investigation show that hyponatremia, polyuria, hyper-natriuresis, besides normo-kalemia are common in the patients with cervical spinal cord injury. All these accord with the manifestations of CSWS even more. We assume that sympathetic nerve system may be inhibited after cervical spinal cord injury[11], then renal diuresis and renal salt wasting occur without the control of renal sympathetic nerve. Additionally, that is also a disturbance of autonomic nervous system after cervical spinal cord injury. Our suggestion needs confirmation with further studies.
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Notwithstanding the mechanism has not been clear. Most authors suggest that the main treatments should be administration with 0.513 mol.L-1 hypertonic NaCl solution and water restriction[5]. Unfortunately, the hyponatremia did not be corrected effectively in spite we administrated the patients with intravenous hypertonic NaCl solution 30 to 60 g per day.
Of the three dead cases, the mean age (63.67 years) was higher than that of this group (41 years). Additionally, the mean developed time (2.67 days) and the mean time of reaching the nadir (11 days) of hyponatremia of the three dead cases were earlier than those (4.49 and 13.61 days) of this group respectively. Furthermore, the mean serum sodium (128.61 mmol.L-1) was less than that of this group (131.43 mmol.L-1). We assume that age, the velocity and degree of hyponatremia development are part of the reason for the death of the hyponatremic patients. Yet it is incapable of making clear the relationship between the patient's age and the development of hyponatremia, because the observed cases were not enough.
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The patients we studied were administrated with intravenous mannitol 2 to 3 weeks and intravenous dexamethasone 5 days. In spite of the fact, that mannitol could increase the excretion of water and electrolytes, and the reabsorption of sodium exceeded that of water. Therefore, mannitol could prevent the rat from acute hyponatremia[12]. It is known that corticosteroid has a mild effect of water and sodium retention. Accordingly, the administration with mannitol and corticosteroid to the patients we studied could not promote the development of hyponatremia.
, 百拇医药
(Edited by WANG Lei)
REFERENCES
1，Frankel HL, Hancock DO, Hyslop G, et al. The value of postural reduction in the initial management of closed injuries of the spine with paraplegia and tetraplegia.I[J]. Paraplegia, 1969，7:179-192
2，Biyani A， Inman CG， el Masry WS. Hyponatraemia after acute spinal injury[J]. Injury， 1993， 24: 671-673
3，Peruzzi WT, Shapiro BA, Meyer PR Jr, et al. Hyponatremia in acute spinal cord injury[J]. Crit Care Med， 1994, 22: 252-258
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4，Zhang Li, Dang GD, Guo ZQ, et al. Cervical spinal cord injury and hyponatremia[J]. Journal of Beijing Medical University(北京医科大学学报)， 1995，27:191-193
5，Zhou GC, Zhao WL, Yuan ZM, et al. Syndrome of inappropriate antidiuratic hormone secretion caused by acute cervical spinal cord injury[J]. Chinese Journal of Spine and Spinal Cord(中国脊柱脊髓杂志)， 1995， 5: 193-196
6，Welt LG, Seldin DW, Nelson WP, et al. Role of the central nervour system in metabolism of electrolytes and water[J]. Arch Int Med, 1952，90:355-378
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7，Wijdicks EF， Vermeulen M， van Brummelen P， et al. Digoxin-like immunoreactive substance in patients with aneurysmal subarachnoid haemorrhage[J]. Br Med J,1987，294:729-732
8，Decaux G, Prospert F, Penninckx R, et al. 5-year treatment of the chronic syndrome of inappropriate secretion of ADH with oral urea[J]. Nephron, 1993，63:468-470
9，Oster JP, Perez GO, Larios O, et al. Cerebral salt wasting in a man with carcinomatous meningitis[J]. Arch Intern Med, 1983，143:2187-2188
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10，Wall BM, Williams HH， Presley DN， et al. Altered sensitivity of osmotically stimulated vasopressin release in quadriplegic subjects[J]. Am J Physiol， 1990，258:R827-35
11，Colachis SC. Autonomic hyperreflexia with spinal cord injury[J]. J Am Paraplegia Soc, 1992，15:3,171-186
12，Gowrishankar M, Chen CB, Cheema-Dhadli S, et al. Prevention of acute hyponatremia by mannitol: an unanticipated mechanism[J]. Clin Nephrol, 1998， 50: 295-300
(Received 2000-03-09), 百拇医药