Elsevier

Surgical Neurology

Volume 68, Issue 4, October 2007, Pages 387-393
Surgical Neurology

Trauma
Hyponatremia in patients with traumatic brain injury: incidence, mechanism, and response to sodium supplementation or retention therapy with hydrocortisone

https://doi.org/10.1016/j.surneu.2006.11.052Get rights and content

Abstract

Background

Hyponatremia is a frequently observed electrolyte abnormality in patients with central nervous system disease. Several mechanisms, such as SIADH, hypopituitarism, and CSWS, have been proposed with varied incidences among several studies. We attempted to clarify the incidence and mechanism of hyponatremia for each type of TBI. We also assessed the efficacy of sodium supplementation and retention therapy. For sodium retention therapy, hydrocortisone was administered, expecting its mineralocorticoid effect, when the hyponatremia was associated with excess natriuresis.

Methods

Retrospective analysis of 298 patients with TBI between January 2003 and December 2004 was performed. The incidence, background, clinical data, and outcome were evaluated.

Results

Of the 298 patients, 50 (16.8%) presented hyponatremia during the time course. Hyponatremia was associated with longer hospital stay (P < .001) and bad outcome (P = .02). Among these 50 patients, 37 recovered from the hyponatremia with simple sodium supplementation. The remaining 13 patients presented massive natriuresis and required additional sodium retention therapy. Hydrocortisone statistically reduced the amount of sodium excretion (P = .002) and returned the serum sodium level to a normal value.

Conclusions

A high rate of hyponatremia after TBI was observed. Further studies are required to establish the precise mechanism of hyponatremia after TBI. Clear definition of CSWS is required to avoid confusion of the pathophysiology that causes hyponatremia. Hydrocortisone was useful to prevent excess natriuresis.

Introduction

Hyponatremia is a frequently confronted electrolyte abnormality in patients after central nervous system disease. Mild hyponatremia induces activity loss and changes in personality, and severe hyponatremia causes seizure attacks, confusion, and even death [1], [42]. Although the SIADH [15], [17], [46], hypopituitarism [6], and CSWS [11], [12], [16], [17], [24], [26], [27], [29], [40], [46] have been reported as causes of hyponatremia, the true mechanism remains unclarified in any central nervous system disease. Hyponatremia after TBI appears to suffer from the greatest lack of understanding, because even the true incidence of hyponatremia in each type of TBI is not known. In the present study, we retrospectively evaluated 298 patients with TBI and clarified the incidence of hyponatremia in each type of TBI, together with the possible causes of hyponatremia. We also assessed the therapeutic value of sodium supplementation therapy and sodium retention therapy. We have previously reported a therapeutic method for improving hyponatremia by mineralocorticoids in patients presenting CSWS after aneurysmal subarachnoid hemorrhage [36], [37]. Thus, for sodium retention therapy, we attempted to administer hydrocortisone, expecting a mineralocorticoid effect, encouraging sodium retention in the kidney.

Section snippets

Patient selection

All medical records between January 2003 and December 2004 were retrospectively screened. Patients admitted with TBI were considered for the study. For analysis, medical charts and radiologic films were used. Patients lacking any abnormal lesions, both neurologically and radiologically, but admitted for observation were excluded. Patients admitted for spinal cord injury and posttraumatic vomiting were also excluded. The patients entered into this study were diagnosed as having one or more of

Patient population and background

In the given period, 298 patients with TBI met the entry criteria. The diagnoses of these patients were as follows: 63 patients with cerebral concussion, 49 patients with skull bone fracture, 8 patients with tSAH, 16 patients with AEDH, 88 patients with CSDH, 23 patients with ASDH, 48 patients with CC, 2 patients with DAI, and 1 patient with traumatic vascular disease. Eight patients had an initial best Glasgow coma scale of lower than 8. The characteristics of the patients are summarized in

Hyponatremia in central nervous system disease

Hyponatremia is frequently observed in stroke [1], [11], [17], [29], [47], brain tumor [1], [17], [27], [40], [47], TBI [1], [12], [15], [17], [24], [25], [46], [47], infectious diseases [1], [16], [17], [47], and other conditions [1], [17], [32], [47]. It is reported to occur also in childhood at a high rate [17], [35], [42]. Hyponatremia lowers the plasma osmotic pressure, which is dangerous for patients with central nervous system disease. Because, in these patients, the low plasma osmotic

Conclusion

A high rate of hyponatremia was observed in patients with TBI. Most of them recovered from the hyponatremia with appropriate fluid therapy; however, some patients who were associated with massive sodium excretion did not. Further studies with assessments of blood volume and pituitary function are needed to clarify the detailed pathophysiology of hyponatremia after TBI. Hydrocortisone was useful for preventing excess natriuresis.

Acknowledgment

This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan (C18591615).

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