ESSENTIALS OF DIAGNOSIS
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 commonly is 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. Acutely, this movement of water can result in cerebral edema, increasing the risk of seizures and even brain herniation.
Chronic hyponatremia is often asymptomatic or present with mild confusion, nausea, or falls. In these patients, cerebral adaptation has occurred as the brain cells have excreted intracellular osmoles to limit cell swelling. In this setting, 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 in reality it usually reflects an excess of total body water. The basic pathophysiologic principle is the ingestion of water (oral or intravenous) in excess of the amount the kidney can excrete is commonly due to the action of ADH. A diagnostic algorithm separates the causes of hyponatremia using serum osmolality, urine sodium, and volume status (Figure 21–1).
A diagnostic algorithm for the causes of hyponatremia using serum osmolality, urine osmolality, and urine sodium. ADH, antidiuretic hormone; GFR, glomerular filtration rate; SIADH, syndrome of inappropriate antidiuretic hormone.
A. Isotonic and Hypertonic Hyponatremia
Hyponatremia is typically associated with hypoosmolality with two exceptions: pseudohyponatremia and hypertonic hyponatremia.
This represents a laboratory artifact that rarely occurs 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 per given volume. This issue is becoming less prevalent as most laboratories are now using direct ion selective electrodes without blood dilution. Consultation with the clinical laboratory is necessary if this condition is suspected.
2. Hypertonic hyponatremia
The best clinical examples of this situation are 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. Note, this leads to a reduction in intracellular volume, and cerebral edema is not caused by hyponatremia in this setting; however, cerebral edema may ...