Cerebral salt wasting after traumatic brain injury: an important critical care treatment issue.

Traumatic brain injury is an important public health issue that requires the expertise of informed neurosurgeons, neurointensivists, and other critical care practitioners. The treatment of patients with traumatic brain injury (TBI) using established guidelines and less well-established novel treatment strategies, including invasive brain monitoring, has led to a silent albeit robust improvement in the outcome after TBI. Rather than adopting a nihilistic posture about TBI, physicians are being called upon to once again champion the care of the patient and to use available treatment measures to facilitate a good outcome. It is truly an exciting time to be caring for patients with TBI in the intensive care unit, and real treatment options do exist. One of the most profound treatment developments in the intensive care of patients with brain trauma has been the focus on identifying and treating hyponatremia as well as inducing a state of hypernatremia among TBI patients with malignant brain edema. For purposes of our current discussion, hyponatremia is operationally defined as a low serum sodium concentration. The actual nominal value of sodium for which hyponatremia is said to exist is not well agreed upon, with various threshold levels of 130, 132, or 135 mmol/L being used in various articles. Using one of more of the threshold values, the incidence of hyponatremia among patients with TBI has ranged from 5% to 10% of patients. However, one must recognize that most patients with TBI will have sodium levels of less than 140 mmol/L. The etiology of the hyponatremia among TBI patients appears to be due primarily to cerebral salt wasting (CSW). Cerebral salt wasting is a condition in which there is an elevation of brain natriuretic peptide (BNP) levels, which results in a reduction in the efficacy of aldosterone and hence a reduction in the ability to reabsorb sodium in the kidney [3]. Brain natriuretic peptide results in an osmotic diuresis in which large amounts of sodium is excreted from the kidney along with free water. The clinical expression of this syndrome is a high urine output of sodium-rich, isotonic, or slightly hypertonic urine, with an elevated specific gravity. Typically the patient will make in excess of 2.5 mL/(kgd h) of urine, with a resultant reduction in total blood volume. If left untreated, CSW can result in