Sodium , serum or plasma (Na+)

135–145 meq/L [mmol/L or mM]

Panic: <125 or > 155 meq/L

SST, green


Physiologic Basis

Sodium homeostasis is crucial for life, and the Na+ level of blood is strictly maintained at a range of 135–145 mM.

Sodium is the predominant extracellular cation. The serum sodium level is primarily determined by the volume status of the individual. Hyponatremia can be divided into hypovolemia, euvolemia, and hypervolemia categories. (See Hyponatremia algorithm, Figure 9–18 .)

Sodium is commonly measured by ion-selective electrode.


Increased in: Dehydration (excessive sweating, severe vomiting, or diarrhea), polyuria (diabetes mellitus, diabetes insipidus), hyperaldosteronism, inadequate water intake (coma, hypothalamic disease). Drugs: steroids, licorice, oral contraceptives.

Decreased in: CHF, cirrhosis, vomiting, diarrhea, exercise, excessive sweating (with replacement of water but not salt, eg, marathon running), salt-losing nephropathy, adrenal insufficiency, nephrotic syndrome, water intoxication, syndrome of inappropriate antidiuretic hormone (SIADH), AIDS. Drugs: thiazides, diuretics, ACE inhibitors, chlorpropamide, carbamazepine, antidepressants (selective serotonin reuptake inhibitors), antipsychotics.


Spurious hyponatremia may be produced by severe lipemia or hyperproteinemia if sodium analysis involves a dilution step.

Many guidelines recommend a correction factor, whereby the serum sodium concentration decreases by 1.6 meq/L for every 100 mg/dL (5.56 mmol/L) rise in plasma glucose above normal, but there is evidence that the decrease may be greater when patients have more severe hyperglycemia (> 400 mg/dL or 22.2 mmol/L) and/or volume depletion. One group has suggested that, when the serum glucose is > 200 mg/dL, the serum sodium concentration decreases by at least 2.4 meq/L.

Hyponatremia in a normovolemic patient with urine osmolality higher than serum (or plasma) osmolality suggests the possibility of SIADH, myxedema, hypopituitarism, or reset osmostat.

Treatment of disorders of sodium balance relies on clinical assessment of the patient’s extracellular fluid volume rather than the serum sodium.

Noda M et al. Sodium sensing in the brain. Pflugers Arch 2015;467:465.  [PMID: 25491503]

Overgaard-Steensen C et al. Clinical review: practical approach to hyponatraemia and hypernatraemia in critically ill patients. Crit Care 2013;17:206.  [PMID: 23672688]

Sam R et al. Understanding hypernatremia. Am J Nephrol 2012; 36:97.  [PMID: 22739333]