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Abstract: PO1144

Use of Tolvaptan to Maintain Eunatremia in Acute Brain Injury-Induced SIADH

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Capistrano, Maria Christina Victoria M., Kent Hospital, Warwick, Rhode Island, United States
  • Shah, Ankur, Brown University Warren Alpert Medical School, Providence, Rhode Island, United States

Eunatremia is a predictor of in-hospital mortality in intracerebral hemorrhage. In hyponatremia from SIADH, usual therapies may not be ideal in patients with stroke. We present a case of hyponatremia from acute brain injury induced SIADH being managed with Tolvaptan.

Case Description

Our patient is a 68 year old man with a history of hypertension who was admitted for an acute hemorrhagic stroke. He had a blood pressure of 204/127 mmHg and an NIHSS of 10. His initial work up shows: glucose 199 mg/dL, creatinine 0.75 mg/dL, Na 137 mmol/L, potassium 3.8 mmol/L, HCO3 of 25 mmol/L, chloride 95 mmol/L. A head CT scan demonstrated a 10 cc right thalamic hemorrhage. He was then started on a nicardipine drip. On the next day, he was noted to have a Na of 129 mmol/L. His serum osmolality, urine osmolality, urine Na were 289 mOSM/kg, 6,783 mOSM/kg and 146 mmol/L respectively. He was given salt tablets with improvement of Na to 131. However, he developed headaches and became hypertensive at 188/94 mmHg. Instead, he was started on a high protein diet, 1 liter fluid restriction and lasix. The next Na level was 129. He was given Tolvaptan 15 mg, which improved the Na to 132, urine osm 645, and urine Na to 12. The dose was increased to 30 mg to achieve eunatremia with these values: Na 135-138, urine Na 12, urine osm 487. His BP improved, tolvaptan was discontinued and salt tablets were resumed. The patient maintained eunatremia throughout the hospital stay.


Hyponatremia is a predictor of mortality due to cellular edema. Eunatremia with Na levels between 135-145 mmol/L is targeted in acute brain injury. SIADH induced by brain injury may be due to an increase in ADH from the overstimulation of the neurohumoral axis. ADH promotes water reabsorption at the cortical and medullary collecting tubules, and inappropriate levels lead to hyponatremia. Tolvaptan is a V2 receptor antagonist which combats this mechanism, thus increasing free water excretion. Additional therapies for hyponatremia from SIADH include fluid restriction, a high protein diet and salt tablets. However, salt tablets increases fluid retention; which increases blood pressurre, and leads to recurrent hemorrhage and poor outcomes. The use of Tolvaptan increases free water excretion to achieve eunatremia, thereby decreasing the risk of brain edema and controls blood pressure, especially in this patient population.