Abstract Introduction: Vasopressin infusion has a crucial role in treating critical care patients needing circulatory support or for maintaining cerebral perfusion in patients with cerebral vasospasm. However, one of the potential side effects of treatment with continuous, high dose of vasopressin is development of diabetes insipidus (DI) at the level of hypothalamus/pituitary and kidneys. Here, we present a case of DI after discontinuing vasopressin infusion in a patient admitted with subarachnoid hemorrhage.Case Presentation: Patient is a 46-year-old male admitted with subarachnoid hemorrhage who underwent emergent balloon-assisted aneurysm coiling and external ventricular drain placement. While in the ICU, he developed elevated intracranial cerebral pressure. Therefore, vasopressin infusion was started for vasospasm treatment with subsequent discontinuation seven days later. The patient then developed significant polyuria and hypernatremia (consistent with DI) shortly after vasopressin infusion discontinuation. Low dose IV DDAVP was then started but he subsequently required higher dosing as high as 1 mcg every 4 hours to maintain normal urine output and serum sodium. Over the next 15 days, DDAVP tapered off with no recurrence of the DI.Conclusions: Vasopressin infusion-induced DI can happen at the level of hypothalamus/pituitary or kidneys. This phenomenon can be explained by depletion of AVP storage in the pituitary gland and/or desensitization of renal ADH receptors due to continuous exposure to supraphysiologic dose of vasopressin. The latter could be overcome by administration of high doses of DDAVP followed by slow tapering to restore receptor sensitization as was the case with our patient.
Rabiei et al. (Fri,) studied this question.