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The underlying mechanism typically involves too little free water in the body. [6] If the onset of hypernatremia was over a few hours, then it can be corrected relatively quickly using intravenous normal saline and 5% dextrose in water. [1] Otherwise, correction should occur slowly with, for those unable to drink water, half-normal saline. [1]
[3] [27] Once the patient is stable, it is important to identify the underlying cause of hypernatremia as that may affect the treatment plan. [3] [27] The final step in treatment is to calculate the patients free water deficit, and to replace it at a steady rate using a combination of oral or IV fluids.
Excessive ADH causes an inappropriate increase in the reabsorption in the kidneys of solute-free water ("free water"): excess water moves from the distal convoluted tubules (DCTs) and collecting tubules of the nephrons – via activation of aquaporins, the site of the ADH receptors – back into the circulation. This has two consequences.
When the body experiences a free water deficit, the concentration of solutes is increased. This leads to a higher serum osmolarity. When serum osmolarity is elevated, this is detected by osmoreceptors in the hypothalamus. These receptors trigger the release of antidiuretic hormone (ADH). [22]
Desmopressin will be ineffective in nephrogenic DI which is treated by reversing the underlying cause (if possible) and replacing the free water deficit. A thiazide diuretic , such as chlorthalidone or hydrochlorothiazide , can be used to create mild hypovolemia which encourages salt and water uptake in proximal tubule and thus improve ...
The resultant value is the approximate volume of free water required to correct a hypernatremic state. In practice, the value rarely approximates the actual amount of free water required to correct a deficit due to insensible losses, urinary output, and differences in water distribution among patients. [13]
Urinary water loss, when the body water homeostat is intact, is a compensatory water loss, correcting any water excess in the body. However, since the kidneys cannot generate water, the thirst reflex is the all-important second effector mechanism of the body water homeostat, correcting any water deficit in the body.
In order to treat diabetes insipidus, the free water deficit must be restored, the missing hormone must be replaced (if central diabetes insipidus is present), and the underlying ailment must be addressed. [8] The medication desmopressin, an arginine vasopressin analogue, is used to treat central diabetes insipidus. [9]