Neuroendocrine Dysfunction

Head trauma places the pituitary gland at risk for injury due to its encasement in the sella turcica, its del­icate infundibular structures, and its tenuous vascular supply. The gland may be subject to edema, ischemia, transection of the pituitary stalk, or watershed injury (163).

DI is commonly noted early after a moderate or severe TBI and can, therefore, be considered a potential marker for global hypothalamo-pituitary injury and dysfunction (164). SIADH also is a result of posterior pituitary dysfunction and needs to be distinguished from DI. The incidence of DI in children is poorly under­stood and poorly researched. One study (165) demon­strated incidence around 21.6% of DI in adults with moderate or severe brain injury. The study also found DI tended to be associated with a lower GCS and with the presence of cerebral edema. The fluid and sodium imbalance of DI results in a deficiency of antidiuretic hormone and excessive water loss. As antidiuretic hor­mone is produced in the hypothalamus, those patients who exhibit DI are felt to be predisposed to other hypo- thalamo-pituitary system dysfunction. Patients with DI are hypernatremic and demonstrate polyuria and poly­dipsia. Although often DI is only a temporary problem for most people with TBI, it may persist. Treatment for DI is desmopressin acetate (DDAVP), which is a syn­thetic form of an antidiuretic hormone (166).

The syndrome of SIADH is another common fluid and electrolyte imbalance encountered in those with TBI, and needs to be distinguished from DI in order to provide appropriate treatment. In contrast to DI, these individuals exhibit decreased urine output, hypona­tremia, and decreased serum osmolarity. SIADH is typically managed with fluid restriction and carefully reestablishing the serum sodium to a normal level in a cautious fashion. Rapid correction of the hypona­tremia can cause pontine myelinolysis and possibly death (166).