Clinical Approach to Euvolemic Hyponatremia

Euvolemic hyponatremia is frequently encountered in hospitalized patients and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause in most patients. SIADH diagnosis is confirmed by decreased serum osmolality, inappropriately elevated urine osmolality (>100 mosmol/L), and elevated urine sodium (Na) levels. Patients should be screened for thiazide use and adrenal or thyroid dysfunction should be ruled out before making a diagnosis of SIADH. Clinical mimics of SIADH like cerebral salt wasting and reset osmostat should be considered in some patients. The distinction between acute (<48 hours) versus chronic (>48 hours or without baseline labs) hyponatremia and clinical symptomatology are important to initiate proper therapy. Acute hyponatremia is a medical emergency and osmotic demyelination syndrome (ODS) occurs commonly when rapidly correcting any chronic hyponatremia. Hypertonic (3%) saline should be used in patients with significant neurologic symptoms and maximal correction of serum Na level should be limited to <8 mEq over 24 hours to prevent the ODS. Simultaneous administration of parenteral desmopressin is one of the best ways to prevent overly rapid Na correction in high-risk patients. Free water restriction combined with increased solute intake (e.g., urea) is the most effective therapy to treat patients with SIADH. 0.9% saline acts as a hypertonic solution in patients with hyponatremia and should be avoided in the treatment of SIADH due to rapid fluctuations in serum Na levels. Dual effects of 0.9% saline resulting in rapid correction of serum Na during infusion (inducing ODS) and post-infusion worsening of serum Na levels are described in the article with clinical examples.