Diabetes Insipidus after Traumatic Brain Injury

Journal of Clinical Medicine

Cristina Capatina¹  Niki Karavitaki²  Alessandro Paluzzi³  Rosalid Mitchell³ 

[1] Carol Davila University of Medicine and Pharmacy, Endocrinology Department,34–36 Aviatorilor Blvd, Bucharest 050474, Romania;Centre for Endocrinology, Diabetes, and Metabolism, Institute for Biomedical Research,School of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK;Neurosurgery, University Hospitals Birmingham NHS Foundation Trust, Queen Elizabeth Hospital, Birmingham, B15 2TH, UK;

关键词: traumatic brain injury;    diabetes insipidus;    hypernatremia;    polyuria;   

DOI  :  10.3390/jcm4071448

来源: DOAJ

【 摘 要 】

Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI.

【 授权许可】

Unknown