Sodium Disorders and Traumatic Brain Injury: A Narrative Review

Traumatic brain injuries (TBI) cause direct central nervous system injury. The presentation depends on the location, the type, and the injury severity. Additional injury may develop secondary to compression, disruption of cerebral perfusion, and changes in sodium levels resulting in either cellular edema or dehydration. Plasma osmolality (Posm) is a critical parameter influenced by solute concentrations, including sodium, glucose, and urea, and is a relevant concern when considering sodium levels in these patients. While Posm can be calculated using a standard formula, direct measurement via osmometry offers better accuracy. It is essential to differentiate between osmolality and tonicity; the latter refers specifically to effective solutes that drive water movement in the extracellular fluid. Sodium and its anions are effective solutes, whereas urea and glucose have variable effects due to their permeability and insulin dependence. Following TBI, dysregulation of osmoregulation may occur and affect neurological outcomes. Osmoreceptors in the brain regulate arginine vasopressin secretion in response to changes in effective solute concentrations, with sodium chloride and mannitol being potent stimuli. The regulation of plasma osmolality, typically maintained within ±5% of a 280-295 mOsm/kg H2O range, is crucial for homeostasis and relies on antidiuresis and thirst mechanisms. This review underscores the complexities of osmoregulation in the context of TBI and its clinical implications, particularly concerning the development of conditions, such as diabetes insipidus, syndrome of inappropriate antidiuretic hormone, and abnormal thirst.