Traumatic brain injury, as a common disease in neurosurgery, refers to the organic damage to the brain tissue caused by severe head trauma (1, 2), with a rather high disability rate and fatality rate. Clinical manifestations include symptoms such as disturbance of consciousness, dizziness, and headache, the delayed treatment for which may give rise to complications such as permanent dysfunction, amnesia, and epilepsy, jeopardizing patients' life safety and hindering the quality of life (3–5). Hyponatremia, defined as serum sodium below 135 mmol/L, is a common complication after traumatic brain injury and often manifests as cerebral salt-wasting syndrome and inappropriate antidiuretic hormone secretion syndrome, which can lead to serious adverse consequences if not treated promptly (6). After traumatic brain injury, the release of anterior pituitary gland adrenocorticotropic hormone increases due to the stress response, which has a certain impact on sodium excretion, and the application of a large amount of dehydrating drugs after traumatic injury can also lead to low sodium, which may cause impaired nerve cell function, resulting in neurological dysfunction and even disability or death in severe cases (7, 8). In addition, patients with traumatic brain injury are frequently complicated with hyponatremia, which may trigger neurological dysfunction or even death and disability in severe cases due to damages to the patients' nerve cells. It has been found clinically that the understanding of the causes of traumatic brain injury complicated by hyponatremia serves to a better prognosis of patients and drives down mortality (9–11). In addition, the clinical treatment of this disease is mainly gastrointestinal sodium supplementation, which has obvious limitations and poor efficacy (12), so it is also urgent to explore more ideal treatment methods. Continuous renal replacement therapy (CRRT) refers to a group of therapeutic techniques for extracorporeal blood purification, which are now widely used in the treatment of critically ill patients with various non-renal diseases (13). It has the advantages of continuous, slow, isotonic and high-volume solute exchange, hemodynamic stability, removal of medium-molecular substances such as inflammatory mediators, and continuous and stable control of electrolyte and acid-base balance (14). To explore the etiology and diagnosis and treatment strategy of traumatic brain injury complicated with hyponatremia, the clinical data of 90 patients with traumatic brain injury admitted to our hospital from 2019 to 2020 were retrospectively analyzed to dissect the etiology, and of the 90 cases included, 50 cases diagnosed with hyponatremia were identified as research objects. The report is as follows:

Brain injury is mainly caused by trauma, with hyponatremia as the most influential factor in the prognosis of the disease (18–20). Currently, most scholars believe that the pathogenesis of traumatic brain injury complicated by hyponatremia is related to abnormal secretion of antidiuretic hormone and cerebral salt wasting syndrome (21, 22). Specifically, brain injury predisposes to brain salt depletion syndrome, leading to increased renal sodium excretion and low sodium reabsorption rates, ultimately leading to excessive sodium secretion and hyponatremia (23). In addition, brain injury also stimulates antidiuretic hormone secretion, which strengthens the renal tubule reabsorption capacity, resulting in a significant decline in blood sodium and then hyponatremia. The complications of hyponatremia in traumatic brain injury may induce symptoms such as irritability, nausea, and lethargy, or even death in severe cases if patients fail to receive effective treatment (24, 25). It has been found clinically that the understanding of the etiology of traumatic brain injury complicated by hyponatremia serves to a better prognosis of patients. In this study, it was found that the cause of traumatic brain injury complicated by hyponatremia was related to the degree of brain injury, ventricular hemorrhage, cerebral edema, and skull base fracture (P < 0.05), which may be attributed to the following factors (26, 27): ① Severe brain injury inhibits the activity of renal sympathetic nerves, thereby increasing the glomerular filtration and causing the reduction of sodium reabsorption in the renal tubules; ② Abnormal secretion of the antidiuretic hormone leads to hyponatremia as symptoms such as intraventricular hemorrhage and cerebral edema trigger blood circulation disorder, hypothalamus damage, and increased intracranial pressure; ③ Cerebrospinal fluid leakage after skull base fracture impairs the patient's hypothalamic function, resulting in hyponatremia. Clinically, most patients with brain injury are complicated with hyponatremia, which aggravates the condition and increases the mortality rate if effective treatment measures are absent. Therefore, in clinical treatment, after diagnosis of cerebral salt wasting syndrome, sodium supplementation was timely provided to maintain a balanced state of electrolytes in the patient's body. However, the treatment approach is conservative and has limitations (28, 29). CRRT can effectively remove solute and water to restore the electrolyte balance. Furthermore, timely adjustment of the replacement fluid Na⁺ according to the patient's blood Na⁺ concentration avoids the imbalance of blood Na⁺ correction speed and reduces the occurrence of excessive blood pressure osmotic fluctuations. In addition to the correction of hyponatremia, continuous renal replacement therapy effectively relieves cerebral edema, removes nitrogen metabolites, reduces osmotic pressure, and maintains the patient's internal environment in a stable state (30). The results of this experiment showed a significantly lower death rate and a lower NSE level of the experimental group after the treatment than the control group (P < 0.05), indicating that the therapy can improve the patient's clinical indicators to reduce mortality. In addition, the present study also found that the GCS score after treatment was higher in the experimental group than in the control group (P < 0.05), and the results of James E (31) et al. stated that “the GCS score after treatment was (14.1 ± 0.73) in the treatment group, which was significantly higher than that of (8.9 ± 0.52) in the control group (P < 0.05)”, which is generally consistent with the results of this study. It fully indicates that CRRT produced significant clinical effects in improving patients' conditions compared with conventional treatment.

In conclusion, the degree of brain injury, ventricular hemorrhage, cerebral edema, and skull base fracture were considered the main factors for traumatic brain injury complicated with hyponatremia. CRRT can effectively improve the clinical indicators of the patients with a promising curative effect, which merits promotion and application.

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.

The studies involving human participants were reviewed and approved by the Ethics Committee of the Affiliated Lianyungang Second People's Hospital of Bengbu Medical College. The patients/participants provided their written informed consent to participate in this study.

JZ is responsible for writing the article. WD is responsible for the design of the study. XD is responsible for the collection of case data. JW and PY are responsible for the recording of the results and statistics. HS is the instructor of the entire study. All authors contributed to the article and approved the submitted version.

This research is supported by the Lianyungang Municipal Health Commission (202120).

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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