Hyponatremia and Hypernatremia

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Chapter 45 Hyponatremia and Hypernatremia

Brad W. Butcher, MD , Kathleen D. Liu, MD, PhD, MAS

1 Why is sodium balance critical to volume control?

Sodium and its corresponding anions represent almost all of the osmotically active solutes in the extracellular fluid under normal conditions. Therefore the serum concentration of sodium reflects the tonicity of body fluids. Small changes in osmolality are counteracted by thirst regulation, antidiuretic hormone (ADH) secretion, and renal concentrating or diluting mechanisms. Preservation of normal serum osmolality (i.e., 285-295 mOsm/L) guarantees cellular integrity by regulating net movement of water across cellular membranes.

2 What is another name for ADH? What is its mechanism of action?

ADH is also called arginine vasopressin or simply vasopressin. ADH is a small peptide hormone produced by the hypothalamus that binds to the vasopressin 1 and 2 receptors (V1 and V2). Vasopressin release is regulated by osmoreceptors in the hypothalamus, which are sensitive to changes in plasma osmolality of as little as 1% to 2%. Under hyperosmolar conditions, osmoreceptor stimulation leads to stimulation of thirst and vasopressin release. These two mechanisms result in increased water intake and retention, respectively. Vasopressin release is also regulated by baroreceptors in the carotid sinus and aortic arch; under conditions of hypovolemia, these receptors stimulate vasopressin release to increase water retention by the kidney. At very high concentrations, vasopressin also causes vascular smooth muscle constriction through the V1 receptor, increasing vascular tone and therefore the blood pressure. Accordingly, vasopressin is often administered parenterally as a vasopressor agent in patients with hypotension that is refractory to volume resuscitation.

3 Does hyponatremia simply mean there is too little sodium in the body?

No. The serum sodium concentration is not a reflection of the total body sodium content; instead, it is more representative of changes in the total body water. With hyponatremia, defined as serum sodium level less than 135 mEq/L, there is too much total body water relative to the amount of total body sodium, thereby lowering its concentration. Despite this key observation, the serum sodium concentration is not a reflection of volume status, and it is possible for hyponatremia to develop in states of volume depletion, euvolemia, and volume excess. Assessing a patient’s volume status is therefore the key step in identifying the underlying cause of hyponatremia (Fig. 45-1). Helpful physical findings include tachycardia, dry mucous membranes, orthostatic hypotension, increased skin turgor (associated with hypovolemia) or edema, an S₃ gallop, jugular venous distention, and ascites (present in hypervolemic states).

Figure 45-1 Diagnostic algorithm for hyponatremia. Na⁺, Sodium concentration.

4 Are hyponatremia and hypoosmolality synonymous?

No. Hyponatremia can occur without a change in total body sodium or total body water in two settings. The first is pseudohyponatremia, which is a laboratory artifact in patients with severe hyperlipidemia or hyperproteinemia. This laboratory abnormality has been essentially eliminated by the use of ion-specific electrodes (rather than flame photometry) to determine the serum sodium concentration. The second setting occurs when large quantities of osmotically active substances (such as glucose or mannitol) cause hyponatremia but not hypoosmolality, a condition known as translocational hyponatremia. In such states, water is drawn out of cells into the extracellular space, diluting the plasma solutes and equilibrating osmolar differences. In addition, use of large quantities of irrigant solutions that do not contain sodium (but instead contain glycine, sorbitol, or mannitol) during gynecologic or urologic surgeries can also cause severe hyponatremia.

5 How can hyponatremia develop in a patient with hypovolemia?

Hypovolemic hyponatremia represents a decrease in total body sodium in excess of a decrease in total body water. Simultaneous sodium and water loss can be due to renal (such as diuretic use) or extrarenal causes. Hypovolemia results in a decrease in renal perfusion, a decrement in the glomerular filtration rate, and an increase in proximal tubule reabsorption of sodium and water; all three mechanisms contribute to decreased water excretion. Furthermore, hypovolemia supersedes the expected inhibition of vasopressin release by hypoosmolality and maintains the secretion of the hormone. In other words, the body protects volume at the expense of osmolality.

6 How does hypervolemic hyponatremia differ from hypovolemic hyponatremia?

In hypervolemic hyponatremia, the kidneys are at the center of the problem because of either intrinsic renal disease or the renal response to extrarenal pathophysiology. Physical examination reveals edema and no evidence of volume depletion. Intrinsic renal disease with a compromised glomerular filtration rate (acute or chronic) prevents adequate excretion of sodium and water. Intake of sodium in excess of what can be excreted leads to hypervolemia (edema), whereas excessive intake of water leads to hyponatremia. In contrast, in congestive heart failure, hepatic cirrhosis, and nephrotic syndrome, the intrinsically normal kidney is stimulated to retain sodium and water in response to perceived decrements in intravascular volume and renal perfusion; as a result, hypervolemia and hyponatremia develop. In general, hypervolemic hyponatremia due to an extrarenal cause is characterized by a low urine sodium concentration (≤ 10-20 mEq/L); this distinguishes it from hypervolemic hyponatremia due to intrinsic renal causes, where the urine sodium is > 20 mEq/L.

7 What is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)?

SIADH is a common cause of euvolemic hyponatremia and is associated with malignancies, pulmonary disease, central nervous system disorders, pain, nausea, and many drugs. Common offending medications include hypoglycemic agents, psychotropics (including antipsychotics and antidepressants), narcotics, and chemotherapeutic agents. Other causes of euvolemic hyponatremia include psychogenic polydipsia, a low-solute diet (beer potomania or the tea and toast diet), hypothyroidism, and adrenal insufficiency.

8 What diagnostic tests are useful in the evaluation of hyponatremia?

The physical examination is critical to the determination of volume status, as previously described. Serum electrolyte and serum and urine osmolality measurements are useful. High urine osmolality despite low serum osmolality suggests either hypovolemic hyponatremia or SIADH if the patient is in a euvolemic state. Very low urine osmolality suggests excessive water intake, as in psychogenic polydipsia or a low-solute diet. Measurements of thyroid-stimulating hormone and cortisol can be used to assess endocrine causes of hyponatremia. As mentioned above, the urine sodium concentration can help distinguish renal and extrarenal causes of hypervolemic hyponatremia.

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