Version July 2025
ALGORITHM —
IMMEDIATE ACTION —
The degree of hyponatremia and the rate of decline of the serum sodium determine acute management. Rapidly identify patients with worrisome clinical features, including:
●Severe hyponatremia (<120 mEq/L [mmol/L]).
●Neurologic manifestations (seizures, obtundation, hyponatremic encephalopathy).
●Acute development (within 24 hours) of hyponatremia, even if neurologic symptoms are mild (headache, nausea).
●Hyperacute development of hyponatremia (within a few hours), even if asymptomatic at the time of presentation.
Patients with severe hyponatremia (<120 mEq/L [mmol/L]) and many symptomatic patients with moderate hyponatremia (121 to 129 mEq/L [mmol/L]) require hospitalization to ensure an appropriate rate of correction. Consultation with a clinician who has expertise in the management of hyponatremia is appropriate for patients under consideration for hypertonic saline to correct their serum sodium. (See "Overview of the treatment of hyponatremia in adults", section on 'Symptomatic (even mild symptoms)'.)
Initiate measures to prevent a further decline in serum sodium, and monitor response to treatment with serial electrolytes. Additional (simultaneous) evaluation is directed at identifying contributing factors. (See 'Initial evaluation' below and "Overview of the treatment of hyponatremia in adults", section on 'Prevent a further decline in serum sodium' and "Diagnostic evaluation of adults with hyponatremia", section on 'The initial evaluation'.)
INITIAL EVALUATION —
The etiology of low sodium can usually be determined from elements of the history, key features of the physical examination, and the results of serum chemistries typically available at the time hyponatremia is identified. The serum sodium concentration generally reflects the tonicity of extracellular fluid. A low serum sodium concentration indicates hypotonicity (table 1), although there are exceptions.
●Assess the patient's volume status.
•Hypervolemia (eg, subcutaneous edema, ascites) suggests advanced liver or cardiac disease. (See "Hyponatremia in patients with heart failure" and "Hyponatremia in patients with cirrhosis".)
•Euvolemia is most commonly associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH).
•Hypovolemia (eg, tachycardia, orthostatic hypotension) is commonly due to gastrointestinal or renal losses.
●Review medications/intravenous fluids that may be contributing to hyponatremia.
●Review prior serum sodium levels if available. If unavailable, repeat serum sodium.
●Review laboratory tests that are usually available at the time that hyponatremia is diagnosed, including:
•Serum glucose (if marked hyperglycemia is present, correct the serum sodium concentration for the effect of glucose (calculator 1)).
•Serum blood urea nitrogen (BUN) and creatinine.
•Serum potassium and bicarbonate.
If the history, physical examination, and initial laboratory tests identify a likely cause (eg, SIADH, cirrhosis, heart failure), additional evaluation may not be required. (See "Diagnostic evaluation of adults with hyponatremia", section on 'The initial evaluation'.)
A normal corrected sodium indicates hyperglycemia-induced hyponatremia. Management requires correction of the hyperglycemia, but it does not require treatment of hyponatremia. (See "Diabetic ketoacidosis in adults: Treatment".)
If the corrected sodium is persistently low, consider/exclude several uncommon clinical scenarios associated with hyponatremia, including the following:
●Suspected nonhypotonic hyponatremia due to exogenous solutes
•Recent treatment with intravenous mannitol.
•Recent use of irrigation solutions during endoscopic urologic, gynecologic, or orthopedic procedures (usually due to glycine accumulation).
•Recent therapeutic intravenous immunoglobulins suspended in hypertonic sucrose or maltose (there may also be a small component of pseudohyponatremia due to the development of hyperproteinemia).
Obtain serum osmolality, which will generally be normal or high (table 2).
●Suspected pseudohyponatremia
•Lipemic serum
•Severe obstructive jaundice (due to lipoprotein X)
•Marked hyperproteinemia (multiple myeloma)
Obtain a concurrent serum osmolality and a plasma sodium level (by direct ion-selective electrode [point of care device or blood gas machine]). In cases of pseudohyponatremia, the serum osmolality and plasma sodium should be normal (table 2).
If the sodium is persistently low and serum osmolality is low (true hypotonic hyponatremia), obtain specialty consultation to aid in the interpretation of results and additional evaluation. The following tests may be indicated to determine the cause of confirmed hypotonic hyponatremia (eg, drugs, gastrointestinal or renal losses, SIADH):
●Urine sodium (to distinguish between occult hypovolemia and euvolemia).
●Urine osmolality (Uosm; to distinguish SIADH from less common causes of hyponatremia such as primary polydipsia or beer potomania, and to identify other causes of hyponatremia that have resolved).
●Thyroid-stimulating hormone (TSH).
●AM cortisol to exclude adrenal insufficiency.
High urine sodium (>40 mEq/L [mmol/L]) and Uosm (usually >300 mOsm/kg) in a patient with clinical euvolemia, no recent diuretic use, and normal renal, thyroid, and adrenal function suggest SIADH. Patients with SIADH require further evaluation of the underlying cause.
REFERENCE RANGE —
The normal reference range for serum sodium is approximately 135 to 146 mEq/L (mmol/L) but can vary depending on the patient population and clinical laboratory. Interpretation of a specific abnormal test result should be based upon the reference range reported with that result.
CITATIONS —
The supporting references for this content are accessible in the linked topics.
