Background: Hyponatremia may complicate brain injury and exacerbate cerebral edema and intracranial pressure (ICP). Vasopressin-receptor antagonists (such as conivaptan) are promising novel agents to treat hyponatremia that act by inducing aquaresis. It is unclear whether raising serum sodium in this way could also confer an acute osmotic benefit, reducing brain water and thereby ICP. We evaluated the effect of a bolus of conivaptan on ICP in a patient with hyponatremia after traumatic brain injury (TBI).
Methods: A 22-year-old suffered severe TBI with occlusive left carotid dissection. Her course was complicated by left hemispheric infarcts with cerebral edema and intermittently elevated ICP. Conivaptan 20-mg IV was given as a bolus when serum sodium rapidly dropped to 128 mEq/l.
Results: This dose resulted in significant aquaresis, with over 1 l per hour of dilute urine peaking at 3-5 h after the dose. By 8 h, sodium had risen to 146 mEq/l. ICP had been stable at 11-15 mmHg for several hours prior to the dose, remained in this range for 2 h after, but then fell to 2 mmHg at 4 h, and remained reduced out to 8 h. Cerebral perfusion pressure, initially stable at 60-80 mmHg, rose to over 90 mmHg at 4 h.
Conclusions: In this preliminary case report, a single dose of conivaptan not only resulted in rapid correction of acute hyponatremia, but also a significant fall in ICP temporally associated with peak aquaresis. Vasopressin-receptor antagonists, by reversing osmotic shifts, may be novel agents to control ICP and cerebral edema, especially in the setting of falling sodium.