A low serum sodium level occurs when there is an excess of extracellular water relative to sodium. Extracellular volume can be high, normal, or low. For most cases of hyponatremia, sodium concentration is decreased as a consequence of either sodium depletion or dilution. 4 Dilutional hyponatremia frequently results from excess extracellular water and therefore is associated with a high extracellular volume status. Either intentional (excessive oral water intake) or iatrogenic (intravenous) excess free water administration can cause hyponatremia. Postoperative patients are particularly prone to increased secretion of antidiuretic hormone, which increases reabsorption of free water from the kidneys with subsequent volume expansion and hyponatremia. This is usually self-limiting in that both hyponatremia and volume expansion decrease antidiuretic hormone secretion. Additionally, a number of drugs can cause water retention and subsequent hyponatremia, such as the antipsychotics and tricyclic antidepressants as well as angiotensin-converting enzyme inhibitors. The elderly are particularly susceptible to drug-induced hyponatremia. Physical signs of volume overload are usually absent and laboratory evaluation reveals hemodilution. Depletional causes of hyponatremia result from either a decreased intake or increased loss of sodium-containing fluids. Etiologies include decreased sodium intake, such as that from a low-sodium diet or enteral feeds that are typically low in sodium, gastrointestinal losses (vomiting, prolonged nasogastric suctioning, or diarrhea), or renal losses (diuretics or primary renal disease). Depletional hyponatremia is often accompanied by extracellular volume deficit.
Hyponatremia can also be seen with an excess of solute relative to free water, such as with untreated hyperglycemia or mannitol administration. Glucose exerts an osmotic force in the extracellular compartment, causing a shift of water from the intracellular to the extracellular space and subsequent dilutional hyponatremia. Hyponatremia can therefore be seen when the effective osmotic pressure of the extracellular compartment is normal or even high. When evaluating hyponatremia in the presence of hyperglycemia, the corrected sodium concentration should be calculated:
FOR EVERY 100-mg/Dl increment in plasma glucose above normal , the plasma sodium decrease by 1.6 mEq/L
Lastly, extreme elevations in plasma lipids and proteins can cause pseudohyponatremia, since there is no true decrease in extracellular sodium relative to water.
Signs and symptoms of hyponatremia (Table 2-3) are dependent upon the degree of hyponatremia and the rapidity with which it occurred. Clinical manifestations are primarily central nervous system in etiology and are related to cellular water intoxication and associated increases in intracranial pressure.
Clinical Manifestations of Abnormalities in Serum Sodium
Central nervous system
Headache, confusion, hyper- or hypoactive deep tendon reflexes, seizures, coma, increased intracranial pressure
Weakness, fatigue, muscle cramps/twitching
Anorexia, nausea, vomiting, watery diarrhea
Hypertension and bradycardia if significant increases in intracranial pressure
To help differentiate the etiology of hyponatremia, a systematic review of the causes of hyponatremia should be undertaken. First, exclude hyperosmolar causes (hyperglycemia or mannitol) and pseudohyponatremia. Next, consider depletional versus dilutional causes of hyponatremia. Depletional causes are usually associated with dehydration. When sodium losses are extrarenal as from gastrointestinal losses, urine sodium levels are usually low (<20 mEq/L), whereas with renal causes of sodium loss, urine sodium levels are usually high (>20 mEq/L). Dilutional causes of hyponatremia are usually associated with a high effective circulating volume. A normal volume status in the case of hyponatremia should prompt an evaluation for a syndrome of inappropriate secretion of antidiuretic hormone.