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Introduction <p>Vasopressin plays a critical role in managing circulatory support and maintaining cerebral perfusion in high-risk neurocritical patients. However, continuous high-dose vasopressin can lead to diabetes insipidus (DI) by affecting the hypothalamus/pituitary or renal ADH receptors. We present a case of DI following vasopressin discontinuation in a patient with subarachnoid hemorrhage (SAH).</p> Case Summary <p>A 46-year-old male presented with SAH and underwent emergency balloon-assisted aneurysm coiling and external ventricular drain placement. During his neuro ICU stay, elevated intracranial pressure prompted initiation of vasopressin infusion to manage suspected cerebral vasospasm. After seven days, vasopressin was discontinued, resulting in significant polyuria and hypernatremia, consistent with DI. The patient was started on IV DDAVP and required escalating doses up to 1 mcg every 4&#xa0;h to control urine output and serum sodium. Over the next 15 days, DDAVP was gradually tapered, with no recurrence of DI symptoms.</p> Conclusion <p>Discontinuation of prolonged vasopressin infusion can lead to transient DI due to pituitary AVP depletion and/or renal receptor desensitization. This condition may require high doses of DDAVP followed by a slow taper to allow restoration of receptor sensitivity and AVP homeostasis.</p>

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Vasopressin Infusion Induced Diabetes Insipidus, a Case Report and Literature Review

  • 期刊论文

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  • 发表日期：

    2026年2月9日

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  • Samaneh Rabiei,
  • Kaye-Anne Newton,
  • Vitaly Kantorovich

摘要

Introduction

Vasopressin plays a critical role in managing circulatory support and maintaining cerebral perfusion in high-risk neurocritical patients. However, continuous high-dose vasopressin can lead to diabetes insipidus (DI) by affecting the hypothalamus/pituitary or renal ADH receptors. We present a case of DI following vasopressin discontinuation in a patient with subarachnoid hemorrhage (SAH).

Case Summary

A 46-year-old male presented with SAH and underwent emergency balloon-assisted aneurysm coiling and external ventricular drain placement. During his neuro ICU stay, elevated intracranial pressure prompted initiation of vasopressin infusion to manage suspected cerebral vasospasm. After seven days, vasopressin was discontinued, resulting in significant polyuria and hypernatremia, consistent with DI. The patient was started on IV DDAVP and required escalating doses up to 1 mcg every 4 h to control urine output and serum sodium. Over the next 15 days, DDAVP was gradually tapered, with no recurrence of DI symptoms.

Conclusion

Discontinuation of prolonged vasopressin infusion can lead to transient DI due to pituitary AVP depletion and/or renal receptor desensitization. This condition may require high doses of DDAVP followed by a slow taper to allow restoration of receptor sensitivity and AVP homeostasis.