One of the most common causes of central diabetes insipidus in children is the neurosurgical destruction of vasopressin neurons after surgery on the hypothalamic-pituitary area. It is important to distinguish polyuria associated with postoperative central diabetes insipidus from polyuria due to normal diuresis of fluids introduced during surgery. In both cases, the urine can be very diluted and in a large volume exceeding 200 ml / m2 / hour. However, in the first case, the serum osmolarity will be high, and in the second – normal. Careful observation in the postoperative period also allows you to distinguish between these two conditions. Vasopressin axons descending from the hypothalamus into the neurohypophysis end at different levels of the pituitary stalk and gland.Since the surgical rupture of these axons can lead to retrograde degeneration of hypothalamic neurons, damage closer to the hypothalamus will damage more neurons and lead to a more pronounced loss of hormone secretion. Often there is a three-phase response. After surgery, there is an initial phase of transient diabetes insipidus, lasts from 1/2 to 2 days, and is the result of swelling of the brain area associated with the normal secretion of vasopressin. If there is a significant destruction of vasopressin cells, a second phase develops, lasting up to 10 days, and characterized by unregulated release of vasopressin by dying neurons. The third phase of persistent diabetes insipidus develops when more than 90% of vasopressin cells are destroyed. In the case of a combined deficiency of vasopressin and cortisol during the surgical treatment of cranio-pharyngioma), the symptoms of diabetes insipidus may be masked, since a deficiency of cortisol violates the clearance of free fluid in the kidneys. In these cases, the appointment of glucocorticoid therapy alone can accelerate polyuria and, accordingly, the diagnosis of diabetes insipidus.
Tumors
Dysgerminoma is one of the most common tumors leading to central diabetes insipidus. Due to the fact that hypothalamic vasopressin neurons are distributed quite widely in the hypothalamus, tumors leading to diabetes insipidus must be either very large in size and infiltratively growing, or strategically located at the junction point of the hypothalamus-neurohypophysical axonal tract in the median elevation. Germinoma and pineoma usually develop near the hypothalamus, where vasopressin axons unite before entering the neurohypophysis, and for this reason are the most common brain tumors associated with diabetes insipidus. Germinomas may be of very small size and not detected on an MRI scan for several years from the onset of polyuria.These tumors often secrete alpha-fetoprotein and / or the beta subunit of human chorionic gonadotropin, which causes premature sexual development in boys. Investigation of the levels of alpha-fetoprotein and the chorionic gonadotropin beta-subunit can help in identifying the supra-malar volume education associated with diabetes insipidus. In this regard, in children with idiopathic diabetes insipidus, it is recommended to conduct a quantitative measurement of human beta-subunit of human chorionic gonadotropin and regular MRI scans of the brain. Empty Turkish saddle syndrome in the outcome of unrecognized pituitary infarction can also be associated with diabetes insipidus.Investigation of the levels of alpha-fetoprotein and the chorionic gonadotropin beta-subunit can help in identifying the supra-malar volume education associated with diabetes insipidus. In this regard, in children with idiopathic diabetes insipidus, it is recommended to conduct a quantitative measurement of human beta-subunit of human chorionic gonadotropin and regular MRI scans of the brain. Empty Turkish saddle syndrome in the outcome of unrecognized pituitary infarction can also be associated with diabetes insipidus.Investigation of the levels of alpha-fetoprotein and the chorionic gonadotropin beta-subunit can help in identifying the supra-malar volume education associated with diabetes insipidus. In this regard, in children with idiopathic diabetes insipidus, it is recommended to conduct a quantitative measurement of human beta-subunit of human chorionic gonadotropin and regular MRI scans of the brain. Empty Turkish saddle syndrome in the outcome of unrecognized pituitary infarction can also be associated with diabetes insipidus.in children with idiopathic diabetes insipidus, it is recommended to carry out quantitative measurement of human beta-subunit human chorionic gonadotropin and regular MRI scans of the brain. Empty Turkish saddle syndrome in the outcome of unrecognized pituitary infarction can also be associated with diabetes insipidus.in children with idiopathic diabetes insipidus, it is recommended to carry out quantitative measurement of human beta-subunit human chorionic gonadotropin and regular MRI scans of the brain. Empty Turkish saddle syndrome in the outcome of unrecognized pituitary infarction can also be associated with diabetes insipidus.
Craniopharyngiomas and gliomas of the optic nerves of large sizes can lead to diabetes insipidus, although in most cases it develops as a result of surgical treatment of these tumors. 10–20% of patients with craniopharyngioma have pronounced diabetes insipidus, and approximately 35% have a partial defect.