Original contribution
Clinical Analysis of Hyponatremia in Acute Craniocerebral Injury

https://doi.org/10.1016/j.jemermed.2008.01.027Get rights and content

Abstract

Objective: To explore pathological mechanisms of central hyponatremia and its treatment. Methods: Synchronous assay was made for changes of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), endogenous digitalis-like substance (EDLS), antidiuretic hormone (ADH) in blood, and Na+ concentrations in blood and urine, and plasma- and urine-osmolality in 68 patients with acute craniocerebral injury (ACI). Results: Of the 68 patients with ACI, 27 were found to have hyponatremia, and such illness was mostly concentrated on severe cases. Conclusions: The central hyponatremia in patients with ACI may be related to the increase in the secretion of EDLS and ADH as the result of damaged functions of the hypothalamic-hypophysial system, and it seems that the decrease in blood ANP and BNP has no direct effect on Na+ concentrations in blood. Inappropriate secretion of antidiuretic hormone syndrome and cerebral salt-wasting syndrome are the two main reasons for hyponatremia in patients with craniocerebral injury. The pathological mechanism, diagnostic standards, as well as treatment methods for the two, however, are not just the same. Intravenous injection of extrinsic thyrotropin-releasing hormone might inhibit dilutional hyponatremia arising from the increase in ADH secretion by patients with ACI.

Introduction

Hyponatremia caused by diseases of the central nervous system is termed central hyponatremia, with a death rate as much as 60 times higher than that for patients without it (1). Because the cause of this disease varies, treatment methods are also different. Therefore, both correct diagnosis and proper treatment have always been a primary concern of neurosurgeons. To explore a new method of treatment for central hyponatremia, we performed pathological analysis of the blood Na+ concentration in the neuroendocrine system in 68 patients with acute craniocerebral injury (ACI), who were studied over the course of 1 year.

Section snippets

Materials and Methods

There were 68 patients (51 male and 17 female) enrolled in the study, with an age range of 4 to 60 years and an average age of 27.8 years. Inclusion criteria included the following: patients hospitalized within 24 h after craniocerebral injury without other severe injuries or shock, and with the diagnosis confirmed by skull computed tomography scan; patients had no history of drinking alcohol before the injury and they had no hypertension or any other heart diseases, with normal function of

Results

A comparison of blood and urine Na+ concentrations and osmotic pressures with varied levels of craniocerebral injuries is presented in Table 1.

The blood osmotic pressure for the ACI group was lower than that for the control group (p < 0.05); however, there was no statistically significant difference in blood osmotic pressure between patients with GCS > 8 vs. those with GCS ≤ 8. The urine osmotic pressure for the ACI group was higher than that for the control group (p < 0.01); however, there was

Discussion

Patients usually have a serious imbalance of water and sodium after severe craniocerebral injuries. The most common result is central hyponatremia, occurring in 31.5% of such patients. Once such an illness occurs, the fatality rate increases by 14.3% (3). After the drop of blood sodium level, patients with severe hyponatremia will become rapidly somnolent with mental confusion or even comatose, and sometimes seizures will occur. If such symptoms are not monitored, identified, and treated in a

Conclusions

When treating traumatic cerebral edema, large doses of dehydrating agents are usually administered, which may increase sodium loss. Therefore, having a clear idea of the components of central hyponatremia and correctly treating it are of vital clinical importance. The focal point in treating SIADH is to restrict fluid intake, whereas the treatment of CSWS is to supplement blood volume and the lost sodium. When sodium can be sufficiently supplemented, use of mineralocorticoid could help recovery

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