In central diabetes insipidus induced by cerebral trauma or following neurosurgery, there is a “triphasic” presentation which may occur. Briefly, the patient begins with a tendency towards hypernatremia, then develops a tendency towards hyponatremia, and finally ends with a chronic tendency towards hypernatremia. The three phases are described below:
- First Phase: due to ischemia or direct trauma to the vasopressin-secreting neurons of the hypothalamus, there is an initial polyuric phase that lasts for about 4-5 days in which there is a fall in urine osmalality and, if the patient loses too much free water, hypernatremia ensues.
- Second Phase: in the second phase, there is a transient SIADH occurring as a result of leakage of vasopressin from damaged posterior pituitary tissue and severed axons. This typically occurs around days 5-6 post-event and the tendency to hyponatremia may be exacerbated by the administration of free water given in response to the First Phase.
- Third Phase: after all the ADH from damaged neurons has leaked out, individuals may or may not enter the third phase, a chronic diabetes insipidus. This does not happen in all individuals as over 80-90% death of all vasopressin-secreting neurons must be destroyed in order for central D.I. to occur.