Endocrine consequences of traumatic brain injury. Literature review

Abstract

Traumatic brain injury (TBI) is associated with increased mortality and morbidity, as well as high rates of longterm disability in survivors. TBI-related deficiencies of both anterior pituitary (posttraumatic hypopituitarism, PTHP) and posterior pituitary (diabetes insipidus PTDI or syndrome of inappropriate antidiuretic secretion, SIADH) are much more frequent than previously known and associated with an unfavourable outcome.The pathophysiology of pituitary dysfunction after TBI is not entirely clear. The traumatic event can induce skull base fractures, hemorrhages or infarction affecting the hypothalamic and pituitary region with consequent endocrine dysfunction. In addition, metabolic and vascular brain changes, frequent in a critically ill patient also aggravate the neuroendocrine dysfunction. In the first days after trauma, the deficiency of adrenocorticotropic hormone and PTDI or SIADH are the main concern because if undiagnosed and untreated are associated with severe dyselectrolitemia and hypotension with increased mortality rate.Posterior pituitary dysfunction occurs in the first days after injury; SIADH usually resolves completely, PTDI can persist in a minority of cases. In contrast, PTHP can occur after a long time interval after TBI. Some degree of PTHP is present in 30-40% of TBI survivors.Early recognition and endocrinological treatment are essential to optimize the outcome of the intensive care management and of the rehabilitation process.