WATER-ELECTROLYTE IMBALANCE IN PATIENTS WITH TRAUMATIC BRAIN INJURY: CLINICAL MANIFESTATION AND TREATMENT

Abstract

Traumatic brain injuries constitute a direct injury to the central nervous system. The presentation depends on the location, type, and severity of the injury. Fluid and electrolyte imbalance are common after traumatic brain injury and may manifest as abnormalities in sodium, potassium, chloride, and calcium levels. Changes in serum sodium levels are the most common and critical electrolyte abnormality. Plasma sodium concentration is a primary determinant of plasma osmolality and is regulated by the secretion of antidiuretic hormone or arginine vasopressin, followed by a sensation of thirst. For decades, disturbances in salt and water balance due to impaired secretion of arginine vasopressin have been observed after traumatic brain injury. This occurrence can manifest as arginine vasopressin deficiency, formerly called central diabetes insipidus, leading to hypernatremia, or arginine vasopressin excess, leading to the syndrome of inappropriate antidiuretic hormone secretion and hyponatremia. Dysnatremia is associated with an increased risk of secondary brain injury due to the resulting changes in brain fluid levels, as well as greater morbidity, and longer hospital stays. Posterior pituitary dysfunction following traumatic brain injury, including alterations in arginine vasopressin release and dysnatremia, most commonly occurs in the acute phase, as it is often transient, and resolves in most patients after recovery from the initial injury. Most importantly, in both hypo and hypernatremia, early detection and prompt appropriate treatment often save lives.