Hydroelectrolytic syndromes in neuroanesthesia and neurocritical care

Electrolyte disorders are pivotal determinants of morbidity and mortality in neurocritical care and exacerbated by acute brain injury, neuroendocrine dysfunction, and therapeutic interventions. This narrative review synthesized contemporary evidence on the pathophysiology, diagnosis, and management of hydroelectrolytic disturbances in neuroanesthesia and neurocritical populations. Dysnatremias (hyponatremia and hypernatremia) are prevalent with emerging data challenging historical correction paradigms: Rapid sodium normalization may reduce mortality without increasing complications. Distinct strategies are required for syndromes of inappropriate antidiuretic hormone secretion (fluid restriction, vaptans) vs cerebral salt wasting (volume resuscitation). Chloride dysregulation, driven by cation-chloride cotransporter imbalances, exacerbates cytotoxic edema and seizures, warranting trials of bumetanide and balanced crystalloids. Hypokalemia, prevalent in traumatic brain injury, demands proactive surveillance to prevent arrhythmias while hyperkalemia management prioritizes membrane stabilization and renal clearance. Hypocalcemia correlates with adverse outcomes in subarachnoid hemorrhage, necessitating timely replacement. Magnesium disorders lack consistent prognostic associations in neurocritical cohorts, contrasting with general critical care. Current evidence underscores the need for individualized, pathophysiology-driven correction, integrating endocrine and neurological principles. Innovations such as point-of-care testing and targeted therapies (e.g., acetate-buffered hypertonic saline) show promise, yet reliance on observational data and preclinical models highlights the urgency for randomized controlled trials. This review advocated for protocolized monitoring, dynamic assessments, and research to define optimal correction thresholds and validate emerging interventions in this high-risk population.