Hyponatremia in septic shock: Pathophysiology, fluid resuscitation challenges, and neurological complications

Sepsis is a life-threatening condition characterized by organ dysfunction due to a dysregulated host response to infection, with septic shock representing its most severe form and carrying high mortality in intensive care units (ICUs). Among critically ill patients, hyponatremia (serum sodium) <135 mmol/L is a common electrolyte disturbance associated with worse outcomes. While prior studies have explored hypernatremia in septic shock, the pathophysiology, clinical implications, and management of hyponatremia in this context remain underexplored, creating uncertainty for clinicians regarding fluid resuscitation strategies and neurological safety. This narrative review aimed to synthesize current evidence on hyponatremia in septic shock, focusing on underlying mechanisms, resuscitation challenges, and neurological complications. A comprehensive literature search was conducted in PubMed, Scopus, Web of Science, EMBASE, and Google Scholar for studies published between 2017 and 2025, including clinical cohorts, case reports, and systematic reviews. The findings indicate that hyponatremia in septic shock arises from non-osmotic vasopressin release, systemic inflammation, acute kidney injury, and fluid shifts during aggressive resuscitation. Large-volume crystalloid administration may exacerbate sodium derangements, while rapid correction poses a risk of osmotic demyelination syndrome (ODS), even under guideline-adherent practices. Case reports suggest plasma exchange may provide the most consistent benefit in severe neurological complications. In conclusion, hyponatremia in septic shock reflects complex neuroendocrine, inflammatory, and renal interactions. Optimized management requires individualized fluid strategies, cautious sodium correction, and prolonged neurological monitoring to mitigate complications and improve outcomes in critically ill patients.