(262) Transient Diabetes Insipidus in a Neonate After Discontinuation of Vasopressin

Introduction: In persistent pulmonary hypertension of the newborn, vasopressin is preferred because it causes selective vasodilation in the pulmonary, renal, coronary, and cerebral vasculature under hypoxic conditions while inducing vasoconstriction in other vascular beds. It lowers right ventricular (RV) afterload, thus improving RV function and resulting in an overall improved cardiac output. Discontinuation of vasopressin leading to transient diabetes insipidus (DI) has been reported in adults. This report presents one case of a neonate with respiratory failure who received vasopressin for hemodynamic support.

Description: Baby PR was born full-term via vaginal delivery with meconium aspiration and respiratory failure, requiring intubation on the day of life (DOL) 1. The patient was transferred to our PICU on the same day, requiring high frequency oscillator ventilator, and subsequently cannulated for ECMO on DOL3. Vasopressin infusion was initiated on DOL2 at shock dosing (0.5-0.6 milliunits/kg/min). During this time, the serum sodium decreased to a nadir of 134 mEq/L, and urine output (UOP) decreased to a nadir of 0.8 ml/kg/hr. After discontinuation on DOL3, the patient developed polyuria (UOP 10-30 ml/kg/hr) and hypernatremia (peak sodium 152 mEq/L). Urine studies revealed low sodium ( < 5 mmol/L) and low urine osmolality (91 mOsm/L). The patient received additional fluid and hypertonic saline boluses due to the electrolyte derangements during this time. Subsequently, the patient was restarted on vasopressin at DI dosing (1.5-2.0 milliunits/kg/hr), resulting in improved urine output. Vasopressin was slowly tapered off by DOL7.

Discussion: We are presenting the first report of transient DI following the discontinuation of vasopressin in neonates. In our case, we reintroduced vasopressin at a lower dose with a slow wean. A likely explanation for DI could be that vasopressin use down regulates anti-diuretic hormone (ADH) production in the hypothalamus, thus disrupting the hypothalamic-pituitary axis and the transport of ADH to the kidneys. This resulted in an acquired form of central DI. Knowledge of this phenomenon can help avoid unnecessary evaluation and may encourage vigilant fluid and sodium administration, as well as a gradual weaning of vasopressin rather than its abrupt discontinuation.