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  • Must know volume status as well as serum and urine osmolality to determine etiology.

  • Hyponatremia usually reflects excess water retention rather than sodium deficiency. The serum sodium concentration is not a measure of total body sodium.

  • Hyponatremia in hospitalized patients is commonly caused by administration of hypotonic fluids.


Hyponatremia is defined as a serum sodium concentration less than 135 mEq/L (135 mmol/L) and is the most common electrolyte abnormality encountered in clinical practice. Hyponatremia represents an excess of water relative to sodium in the plasma leading to a reduction in plasma osmolality and subsequent movement of water from the extracellular fluid into the intracellular fluid. If this movement of water happens too acutely, cerebral edema can occur, increasing the risk of seizures and even brain herniation.

Chronic hyponatremia is often asymptomatic or present with mild confusion, nausea, or falls; cerebral adaptation occurs as the brain cells excrete intracellular osmoles to limit cell swelling. In this setting, hyponatremia must be corrected slowly. Over-rapid correction of chronic hyponatremia may produce profound neurologic abnormalities (osmotic demyelination syndrome).

A common misconception is that hyponatremia is secondary to a deficiency in total body sodium, when this state actually usually reflects an excess of total body water. The basic pathophysiologic principle is that more water (oral or intravenous) is ingested than the kidney can excrete (commonly due to the action of ADH). A diagnostic algorithm (Figure 23–1) separates the causes of hyponatremia using serum osmolality, urine sodium, and volume.

Figure 23–1.

A diagnostic algorithm for the causes of hyponatremia using serum osmolality, urine osmolality, and urine sodium.


A. Isotonic and Hypertonic Hyponatremia

Hyponatremia is typically associated with hypoosmolality with two exceptions: pseudohyponatremia and hypertonic hyponatremia.

1. Pseudohyponatremia

This represents a rare laboratory artifact in patients with marked hypertriglyceridemia or hypergammaglobulinemia. In these settings, there is an increase in the solid components of plasma, relative to plasma water, resulting in a lower sodium level per given volume. This issue has become less prevalent since most laboratories use direct ion selective electrodes without blood dilution. Consult the clinical laboratory if this condition is suspected.

2. Hypertonic hyponatremia

The best clinical examples of this situation occur in the setting of hyperglycemia, and less commonly, mannitol infusion. Both glucose and mannitol are active osmoles, increasing the osmolality of the extracellular fluid, which pulls water from inside cells into the extracellular space, diluting the sodium content. Note, this leads to a reduction in intracellular volume, and cerebral edema is therefore not caused by hyponatremia in this setting. However, cerebral edema may occur in the treatment phase ...

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