Desmopressin, a synthetic
vasopressin analog, is used to treat
central diabetes insipidus,
hemostatic disorders such as
von Willebrand's disease, and
nocturnal enuresis. We present the case of a 69-year-old man who developed severe
hyponatremia during treatment with intranasal
desmopressin at 10 µg twice daily for chronic
polyuria and
nocturia thought to be due to
central diabetes insipidus. After 5 months of
therapy, the patient noticed progressive
fatigue,
anorexia,
dizziness, weakness,
light-headedness, decreased concentration, and new-onset falls. At 6 months of
therapy, the patient was brought to the emergency department for altered mental status and was found to be severely hyponatremic with a serum
sodium level of 96 mmol/L, down from a value of 134 mmol/L at the initiation of
therapy. The intranasal
desmopressin was discontinued and the patient was admitted to the intensive care unit where the
hyponatremia was slowly corrected over the next week to 132 mmol/L, never increasing by more than 8 mmol/L a day, with careful fluid management. This included infusion of over 11 L of 5%
dextrose to account for a high urine output, which peaked at 7.4 L in 1 day. However, while the recommended rate for
sodium correction was followed, the patient's magnetic resonance imaging of the brain obtained after discharge displayed evidence of
central pontine myelinolysis. Despite this finding, the patient eventually returned to his baseline mental status with no permanent
neurologic deficits.