Electrolyte imbalances are common among patients with traumatic brain injury (TBI). Cerebral salt wasting (CSW) is an electrolyte imbalance characterized by hyponatremia and hypovolemia. Differentiating the syndrome of inappropriate antidiuretic hormone and CSW remains difficult and the pathophysiological mechanisms underlying CSW are unclear. Our intent was to review the literature on CSW with...

S sodium levels in critically ill patients can be altered by many factors. The human body is 60% to 70% water, with approximately 30% of that water as extracellular fluid and sodium chloride as the major electrolyte (135-145 mEq/L). Hypo natremia occurs when a person’s serum sodium level is less than 135 mEq/L; it is the most common electrolyte abnormality among hospitalized patients, occurring...

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...

Hyponatremia has been recognized as an important postoperative metabolic complication after central nervous system (CNS) operations in children. If not appropriately treated, the postoperative hyponatremia can cause several types of CNS and circulatory disorders such as cerebral edema, increased intracranial pressure. The postoperative hyponatremia after CNS surgery has been considered as one o...

The epithelial Na+ channel (ENaC) controls the rate-limiting step in the process of transepithelial Na+ reabsorption in the distal nephron, the distal colon, and the airways. Hereditary salt-losing syndromes have been ascribed to loss of function mutations in the α-, β-, or γ-ENaC subunit genes, whereas gain of function mutations (located in the COOH terminus of the β- or γ-subunit) result in h...

The reabsorption of salt in the distal nephron is predominantly mediated via the thiazide-sensitive sodium chroride cotransporter, NCC (SLC12A3), and the chloride-bicarbonate exchanger pendrin (SLC26A4, PDS), with pendrin working in tandem with the epithelial sodium channel and NCC working by itself. Single deletion of NCC or pendrin in genetically engineered mouse models does not cause salt wa...