Urea for treatment of acute SIADH in patients with subarachnoid hemorrhage: a single-center experience

This is a retrospective analysis of all patients admitted to our department for nontraumatic SAH between January 2003 and December 2008 (n？=？368). All patients with SIADH-induced hyponatremia (plasma sodium？<？135 mEq/L, urine sodium？>？20 mEq/L, and osmolality？>？200 mOsm/kg; absence of overt dehydration or hypovolemia; no peripheral edema or renal failure; no history of adrenal or thyroid disease) routinely received urea per os when hyponatremia was associated with clinical deterioration or remained less than 130 mEq/L despite saline solution administration.Forty-two patients developed SIADH and were treated with urea. Urea was started after a median of 7 (IQR, 5–10) days and given orally at doses of 15–30 g tid or qid for a median of 5 (IQR, 3–7) days. The median plasma sodium increase over the first day of treatment was 3 (IQR, 1–6) mEq/L. Hyponatremia was corrected in all patients, with median times to Na+ >130 and >135 mEq/L of 1 (IQR, 1–2) and 3 (IQR, 2–4) days, respectively. Urea was well tolerated, and no adverse effects were reported.Oral urea is an effective and well-tolerated treatment for SIADH-induced hyponatremia in SAH patients.