Diabetes insipidus after traumatic brain injury

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Diabetes insipidus after traumatic brain injury. / Capatina, Cristina; Paluzzi, Alessandro; Mitchell, Rosalid; Karavitaki, Niki.

In: Journal of Clinical Medicine, Vol. 4, No. 7, 13.07.2015, p. 1448-62.

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Capatina, Cristina ; Paluzzi, Alessandro ; Mitchell, Rosalid ; Karavitaki, Niki. / Diabetes insipidus after traumatic brain injury. In: Journal of Clinical Medicine. 2015 ; Vol. 4, No. 7. pp. 1448-62.

Bibtex

@article{d267717aa16d4668a6bc612fe567ec16,
title = "Diabetes insipidus after traumatic brain injury",
abstract = "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.",
keywords = "traumatic brain injury, diabetes insipidus, hypernatremia, polyuria",
author = "Cristina Capatina and Alessandro Paluzzi and Rosalid Mitchell and Niki Karavitaki",
year = "2015",
month = jul,
day = "13",
doi = "10.3390/jcm4071448",
language = "English",
volume = "4",
pages = "1448--62",
journal = "Journal of Clinical Medicine",
issn = "2077-0383",
publisher = "MDPI",
number = "7",

}

RIS

TY - JOUR

T1 - Diabetes insipidus after traumatic brain injury

AU - Capatina, Cristina

AU - Paluzzi, Alessandro

AU - Mitchell, Rosalid

AU - Karavitaki, Niki

PY - 2015/7/13

Y1 - 2015/7/13

N2 - 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.

AB - 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.

KW - traumatic brain injury

KW - diabetes insipidus

KW - hypernatremia

KW - polyuria

U2 - 10.3390/jcm4071448

DO - 10.3390/jcm4071448

M3 - Article

C2 - 26239685

VL - 4

SP - 1448

EP - 1462

JO - Journal of Clinical Medicine

JF - Journal of Clinical Medicine

SN - 2077-0383

IS - 7

ER -