Traumatic brain injury (TBI) accounts for 50% of deaths from bodily injury and of those who survive many suffer long-term functional disability. Serum sodium disorders are frequently encountered in patients with traumatic brain injury (TBI) during the ICU stay. In this clinical setting, a proportion of the cases of hypernatremia is probably due to the onset of central diabetes insipidus (CDI) – an independent marker of brain injury severity and an independent prognostic indicator of ICU death. Be this and/or other mechanisms at play, hypernatremia is anyhow independently related with an increased risk of death.1 TBI is classified as Mild, Moderate, Severe based on GCS, A GCS score ≤ 8 means severe TBI, 9 to 12 means moderate TBI, and 13 to 15 means mild TBI.2 Sodium is the major extracellular cation and one of the most important osmotically active solutes. The extracellular to intracellular fluid sodium concentration gradient is maintained by the sodium–potassium ATPase pump and total body sodium is controlled by renal excretion. Sodium is freely filtered at the glomerulus and the majority is reabsorbed at the proximal tubule under the control of sympathetic nerves and atrial (ANP) and brain (BNP) natriuretic peptides.3 Sodium disturbances are common in patients with brain injury because of the major role that the central nervous system plays in the regulation of sodium and water homeostasis. In addition, treatment of the injured brain can itself disturb regulation of sodium and water. Sodium disturbances can lead to serious complications and adverse outcomes, including death.4 Hyponatraemia is defined as a serum sodium concentration of less than 135 mmol/litre and occurs in up to 15% of the general adult inpatient population. It is more common after brain injury, especially in those patients who are critically ill.5 Hypernatraemia is defined as a serum sodium of 145 mmol/litre. It occurs less commonly than hyponatraemia; its incidence is ~1% in the general inpatient hospital population and 9% in the intensive care setting. It is more common in brain-injured patients and is often an indicator of the severity of the underlying disease.6 In a study done by Deveduthras et al. on patients with moderate and severe head injury the prevalence of abnormal serum sodium concentrations was almost 69% of whom almost half had hyponatremia and the rest hypernatremia. The analysis of the onset of sodium abnormality showed that for those patients who survived, a later onset was related to a better outcome. This makes early diagnosis of abnormal serum sodium important to identify and treat the underlying cause. An early screening tool should be in place in all critical care units where moderate to severe TBI is managed to establish if serum sodium is abnormal, for example, regular blood gas measurements with electrolytes. A controlled fluid management protocol is required at both referral hospitals and in the ongoing management of these patients with moderate to severe TBI to reduce the prevalence of sodium abnormalities.7 The Glasgow Outcome Scale (GOS) was first published in 1975 by Bryan Jennett and Michael Bond. The GOS was devised to provide an overview of outcome and to focus on social recovery. The enduring appeal of the GOS is linked to its simplicity, short administration time, reliability and validity, stability, flexibility of administration.8 This study was planned to see the relationship between sodium abnormality, diagnosis and outcome in patients admitted in neurosurgery icu with traumatic brain injury patients and to find out if the onset of sodium abnormality has any effect on the outcome of the patient. Aim To study the effect of serum sodium in TBI patients and their clinical outcome Objectives: To study the serum sodium levels and outcome of management in TBI

Study Design and Setting This was an observational, cross-sectional, retrospective study conducted in the Department of Neurosurgery, Christian Medical College (CMC), Ludhiana, a tertiary care referral center. The study involved a review of medical records over a two-year period, from 1 July 2018 to 30 June 2020. Study Population All patients admitted to the Neurosurgery Intensive Care Unit (ICU) with a diagnosis of traumatic brain injury (TBI) during the study period were considered eligible for inclusion. Patients of all age groups and both sexes were included to ensure broad representation of the TBI population managed at the institute. Inclusion and Exclusion Criteria Inclusion criteria comprised all patients admitted to the neurosurgery ICU with a confirmed diagnosis of TBI during the study period. Exclusion criteria included patients with associated high cervical spine injuries, as such injuries can independently influence neurological outcomes and confound the assessment of outcome related solely to TBI. Data Collection Data were collected retrospectively from hospital medical records and the Hospital Information Management System (HIMS). Demographic variables including age and sex were recorded. Clinical data included mechanism of injury, presenting symptoms, and Glasgow Coma Scale (GCS) score at admission, which was used to categorize TBI severity as mild (GCS 13–15), moderate (GCS 9–12), or severe (GCS ≤8). Assessment of Serum Sodium Levels Serum sodium values were obtained from the Biochemistry Department HIMS records. All serum sodium measurements performed within the first seven days of ICU admission were documented for each patient. Sodium levels were categorized as hyponatremia (<135 mmol/L), normonatremia (135–144 mmol/L), and hypernatremia (≥145 mmol/L). For analysis, the presence of any sodium abnormality during the first week of admission was considered. Outcome Assessment Neurological outcome was assessed at the time of hospital discharge using the Glasgow Outcome Scale (GOS). Outcomes were categorized into five groups: death, vegetative state, severe disability, moderate disability, and good recovery. The relationship between serum sodium levels and clinical outcomes was evaluated. Sample Size Calculation The sample size was calculated based on a previous study by Devuduthras et al., which reported a 38% prevalence of hypernatremia in patients with severe TBI. Using a confidence level of 95%, an absolute precision of 5%, and a design effect (DEFF) of 1, the minimum calculated sample size was 360 patients. Considering the study duration and availability of records, all eligible patients admitted during the two-year period were included, resulting in a final sample size of up to 600 patients. Statistical Analysis Data were entered into Microsoft Excel and analyzed using Statistical Package for the Social Sciences (SPSS) version 26.0. Continuous variables were expressed as mean ± standard deviation (SD), while categorical variables were summarized as frequencies and percentages. Associations between serum sodium levels and categorical variables, including GOS outcomes, were analyzed using appropriate statistical tests. A p-value <0.05 was considered statistically significant. Ethical Considerations As this was a retrospective record-based study, individual patient consent was waived. The study protocol was conducted in accordance with institutional ethical standards and maintained strict confidentiality of patient data.

There were 533 patients who presented with Traumatic Brain injury, with majority 440(82.6%) males and 93(17.4%) females. The mean age group of presentation was in the age group 32 ± 17. The Majority of patients had Mild Head Injury 366 (68.7%), with Moderate Head Injury in 75(14.1%), and severe head injury in 92 (17.3%). The Mean GCS of the patients was 12.5 ± 3.5. Sodium was normal in majority 355 (66.6%) patients, with moderate hyponatremia in 9(1.7%) patients, Mild Hyponatremia in 160 (30%) of patients. Hypernatremia was noted in 9(1.7%) of total patients. Mean Sodium in the study was 136.9 ± 3.96. Majority of the patients had Moderate disability with GOS 4 in 452(84.8%) of people with Good recovery in 40(7.5%), Severe disability in 12 (2.3%), Neuro vegetative state 7(1.3%), Death in 22(4.1%) of all the patients recruited in the study. There was significant statistical relationship between the serum sodium value and the GOS outcome Table 1: GCS and serum sodium levels on admission among all traumatic brain injury cases Mean ± SD Age 32 ± 17 GCS category 12.5 ± 3.5 Serum Na value 136.9 ± 3.96 Table 2: Characterization of patients based on sodium levels in various groups Hyponatremia Normal Hypernatremia TOTAL Age 0 – 14 years (Pediatric) 25 (37.3%) 41 (61.2%) 1 (1.5%) 67(12.6%) 15 – 47 years (young age) 109 (30.5%) 244 (68.3%) 4 (1.1%) 357(67.0%) 48 – 63 years (middle age) 24 (30%) 53 (66.3%) 3 (3.8%) 80(15.0%) ≥ 64 years (elderly) 11 (37.9%) 17 (58.6%) 1 (3.4%) 29(5.4%) Gender Females 29 (31.2%) 62 (66.7%) 2 (2.2%) 93 (17.4%) Males 140 (31.8%) 293 (66.6%) 7 (1.6%) 440 (82.6%) Type of head injury Mild 107 (29.2%) 256 (69.9%) 3 (0.8%) 366 (68.7%) Moderate 22 (29.3%) 49 (65.3%) 4 (5.3%) 75 (14.1%) Severe 40 (43.5%) 50 (54.3%) 2 (2.2%) 92 (17.3%) GCS Mild 22 (25%) 66 (75%) 0 (0%) 88 (16.5%) Moderate 26 (30.6%) 57 (67.1%) 2 (2.4%) 85 (15.9%) Severe 121 (33.6%) 232 (64.4%) 7 (1.9%) 360 (67.5%) Injury Fall 41 (34.5%) 74 (62.2%) 4 (3.4%) 119 (22.3%) Assault 18 (24.7%) 55 (75.3%) 0 (0%) 73 (13.7%) Firearm injury 2 (100%) 0 (0%) 0 (0%) 2 (0.4%) Road Traffic Accident 107 (31.8%) 225 (66.8%) 5 (1.5%) 337 (63.2%) Unknown 1 (50%) 1 (50%) 0 (0%) 2 (0.4%) Loss of consciousness 107 (31.6%) 225 (66.4%) 7 (2.1%) 339 (63.6%) Seizure 18 (29%) 43 (69.4%) 1 (1.6%) 62 (11.6%) Vomiting 59 (29.6%) 139 (69.8%) 1 (0.5%) 199 (37.3%) GOS at discharge Dead 6 (27.3%) 15 (68.2%) 1 (4.5%) 22 (4.1%) Neurovegetative state 1 (14.3%) 6 (85.7%) 0 (0%) 7 (1.3%) Severe Disability 6 (50%) 6 (50%) 0 (0%) 12 (2.3%) Moderate disability 151 (33.4%) 293 (64.8%) 8 (1.8%) 452 (84.8%) Good recovery 5 (12.5%) 35 (87.5%) 0 (0%) 40 (7.5%) Table 3: Characterization of patients based on GOS score and their mean sodium levels on admission using ANOVA (p= 0.008) GOS n Mean Na level Dead 22 138.136 ± 4.33 Neurovegetative state 7 139.714 ± 2.98 Severe Disability 12 135.917 ±2.96 Moderate disability 452 136.704 ±4.03 Good recovery 40 138.475 ±2.71 Total 533 136.917 ±3.96 Results: There were 533 patients with 440(82.6%) males and 93( 17.4%) females. Sodium was normal in 355 (66.6%) patients, with moderate hyponatremia in 9(1.7%) patients. Mild Hyponatremia in 160 (30%) of patients. Hypernatremia was noted in 9(1.7%) of total patients. The Majority of patients had Mild Head Injury 366 (68.7%), Moderate Head Injury 75(14.1%), severe head injury (17.3%) Moderate disability with GOS 4 in majority 452(84.8%) of people with Good recovery in 40(7.5%), Severe disability in 12 (2.3%), Neuro vegetative state 7(1.3%), Dead 22(4.1%) of all the patients recruited in the study. There was significant statistical relationship between the serum sodium value and the GOS outcome (P <=0.008)

Traumatic brain injury (TBI) continues to represent a major global health burden, accounting for a substantial proportion of injury-related mortality and long-term neurological disability.¹ Advances in neurocritical care have improved survival; however, secondary brain injury due to systemic and metabolic derangements remains a major determinant of outcome. Among these, disorders of serum sodium are particularly important because of their direct effects on cerebral edema, intracranial pressure, and neuronal function.²⁻⁴ In the present study, serum sodium abnormalities were observed in nearly one-third of patients admitted with TBI, with hyponatremia being considerably more common than hypernatremia. This finding is consistent with earlier and contemporary studies reporting dysnatremia as one of the most frequent electrolyte disturbances in neurocritical care units.⁴⁻⁶ The predominance of hyponatremia may be attributed to hypothalamic–pituitary dysfunction following brain injury, leading to conditions such as syndrome of inappropriate antidiuretic hormone secretion (SIADH) and cerebral salt wasting (CSW).⁵⁻⁷ Both entities are well-recognized complications of TBI and are associated with increased morbidity if not promptly identified and treated. Hypernatremia, although less frequent in our cohort, remains clinically significant. Previous studies have demonstrated that hypernatremia in TBI patients is often associated with central diabetes insipidus (CDI), aggressive osmotherapy, inadequate free water intake, or impaired thirst mechanisms.⁸⁻¹⁰ Importantly, CDI has been identified as an independent marker of injury severity and a strong predictor of mortality in patients with severe TBI.⁸⁻¹¹ Even in the absence of overt CDI, hypernatremia has been independently associated with increased ICU mortality and prolonged hospital stay.⁹⁻¹² A key finding of this study was the statistically significant association between serum sodium levels and neurological outcome as assessed by the Glasgow Outcome Scale (GOS). Patients with poorer outcomes—including death, vegetative state, and severe disability—had higher mean serum sodium levels compared to those with good recovery. This observation aligns with multiple large observational studies and meta-analyses demonstrating that both hypo- and hypernatremia are independently associated with unfavorable neurological outcomes and increased mortality in TBI patients.⁶⁻¹³⁻¹⁵ The pathophysiological basis for this association is multifactorial. Hyponatremia can exacerbate cerebral edema by promoting water movement into injured brain tissue, thereby increasing intracranial pressure and reducing cerebral perfusion.⁴⁻⁶ Conversely, hypernatremia may lead to neuronal dehydration, cerebral vasoconstriction, and osmotic demyelination, particularly when correction is rapid or uncontrolled.¹⁰⁻¹² These mechanisms underscore the importance of maintaining strict sodium homeostasis during the acute and subacute phases of brain injury. Our findings are comparable with a study, who reported sodium abnormalities in nearly 69% of patients with moderate to severe TBI and demonstrated that early-onset dysnatremia was associated with worse outcomes.⁷ More recent studies have reinforced this observation, emphasizing that early electrolyte disturbances reflect the severity of primary brain injury and contribute to secondary brain damage if inadequately managed.¹⁴⁻¹⁶ Consequently, early and frequent monitoring of serum sodium, particularly during the first week of ICU admission, has been recommended in contemporary neurocritical care guidelines.³⁻⁴ The clinical implications of this study are significant, as sodium disturbances represent potentially modifiable risk factors. Protocol-driven fluid therapy, judicious use of hyperosmolar agents, early identification of endocrine dysfunction, and individualized correction strategies may help mitigate secondary brain injury and improve neurological outcomes.¹⁵⁻¹⁷ Incorporating routine electrolyte surveillance into standardized TBI management bundles could therefore have a meaningful impact on patient outcomes, especially in resource-limited settings. The use of the Glasgow Outcome Scale in this study allowed standardized assessment of functional outcome and facilitated comparison with existing literature.¹⁸ However, while GOS is widely validated and practical, it does not capture subtle cognitive or neuropsychological deficits. Future studies employing extended outcome scales, such as the Glasgow Outcome Scale–Extended (GOS-E), and longer follow-up periods may provide deeper insight into the long-term impact of sodium disturbances after TBI.¹⁸⁻¹⁹further morbidity and mortality. Limitations This study has certain limitations. Its observational design precludes causal inference. The retrospective nature of data collection limited detailed differentiation between etiologies of sodium disturbances, such as SIADH, CSW, or CDI. Additionally, long-term outcomes beyond hospital discharge were not assessed. Despite these limitations, the large sample size and real-world ICU data strengthen the clinical relevance of the findings. Future Directions Future studies should involve prospective, multicenter designs with standardized electrolyte monitoring to better define the temporal relationship between serum sodium disturbances and outcomes in traumatic brain injury (TBI). Differentiation of etiologies such as syndrome of inappropriate antidiuretic hormone secretion, cerebral salt wasting, and central diabetes insipidus using uniform diagnostic criteria is needed to enable targeted management. Interventional trials evaluating protocol-based fluid and electrolyte strategies may help determine whether early correction of dysnatremia improves neurological outcomes. Incorporating extended outcome measures such as the Glasgow Outcome Scale–Extended and long-term follow-up will provide a more comprehensive assessment of recovery. Finally, evaluating cost-effective screening and monitoring strategies is essential, particularly in resource-limited settings.

Serum sodium abnormalities are common in patients with traumatic brain injury and are significantly associated with neurological outcomes at discharge. Both hyponatremia and hypernatremia contribute to adverse outcomes, with hypernatremia showing a stronger association with mortality and severe disability. Early detection, close monitoring, and timely correction of sodium disturbances should be integral components of comprehensive TBI management protocols to improve patient outcome.

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