Hyponatremia is a disorder of hypo-osmolality in which the rate of sodium loss exceeds the rate of water loss (true hyponatremia). Another type of hyponatremia, relative hyponatremia, is a condition in which the rate of water intake exceeds the kidneys’ ability to secrete free water and maximally dilute the urine. Hyponatremia is characterized by a low serum sodium level and a low serum osmolality. It is a very common electrolyte disorder (Palm et al., 2006; Siragy, 2006).

Hyponatremia occurs in patients with malignancies (Elejalde, 2004) and in those who are hospitalized and institutionalized. It is most frequently seen in elderly individuals. If the condition goes untreated or undiagnosed, many serious outcomes are possible. These consequences often are neurologic in nature and may include seizures, cerebral edema, apnea, coma, and death.

Hypotonic hyponatremia can be classified as euvolemic, hypervolemic, or hypovolemic based on an assessment of the serum sodium level, the serum and urine osmolality, and the body’s fluid volume status.

Euvolemic hyponatremia occurs when the body retains too much electrolyte free water. This type of hyponatremia normally is related to impaired renal excretion in renal failure and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) (see Chapter 47).

Hypervolemic hyponatremia occurs with an increase in the extracellular fluid volume. It usually is accompanied by a disease process, such as heart failure.

Hypovolemic hyponatremia is related to a decrease in the extracellular volume as a result of renal sodium wasting, which leads to cerebral salt wasting (CSW), such as can occur in patients with subarachnoid hemorrhage. The CSW likely related is to decreased secretion of brain natriuretic peptide, with a resulting decrease in the secretion of aldosterone. If the condition goes untreated, cerebral edema occurs, with neurologic compromise and potential herniation of the brain. Hypovolemic hyponatremia also can be caused by conditions in which the body’s need to replace intravascular volume outweighs the need to maintain appropriate serum and blood osmolality.

In all cases, the hyponatremia can lead to impaired cognitive function, a depressed level of consciousness, and convulsions.

In summary, hypotonic hyponatremia can be euvolemic (diuretic therapy, SIADH), hypervolemic (heart failure, cirrhosis, renal failure) or hypovolemic (CSW). It also can have the major clinical presentation of cerebral edema caused by water entering the brain.

A common cause of hyponatremia is hyperglycemia, which raises the plasma osmolality while sodium levels remain the same; this has the effect of lowering the plasma sodium concentration. Heart failure reduces the serum osmolality while raising the extracellular fluid volume, leading to hyponatremia.

Hormones are also involved with water balance regulation; these include antidiuretic hormone (ADH), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and c-type natriuretic peptide (CNP). ADH, also known as arginine vasopressin (AVP), is produced by the hypothalamic nuclei in response to increased plasma osmolality and decreased vascular volume. It acts on the distal tubules and collecting ducts of the nephrons to increase free water permeability and reabsorption of free water and promotes vasoconstriction. ANP is secreted mainly from the atria of the heart in response to atrial stretch caused by elevated intravascular volume or systolic heart failure. BNP is present in the brain and cardiac ventricles and is elevated in patients with cardiac hypertrophy or heart failure. C-type peptides promote shifting of fluid from the intravascular compartments to the extravascular compartments, thereby reducing blood pressure. As can easily be seen, if any of these hormone levels are altered, the resulting fluid volume changes can have serious consequences. In oncology patients, hyponatremia also can result from SIADH (see Chapter 47), which produces an overall euvolemic or mild hypervolemic state, and from CSW, which results in an overall hypovolemic state with compensatory tachycardia.

Hyponatremia occurs in 1% to 2% of hospitalized patients (Offenstandt & Das, 2006) and in these cases is known as hospital-acquired hyponatremia (Moritz & Ayus, 2006). It is the second most common problem in oncology patients (Elejalde, 2004), and it occurs in 31.3% of institutionalized elderly individuals (Chen et al., 2006). Hyponatremia often is caused by overadministration of hypotonic intravenous fluids after surgery; this complicates the condition of 20% of all surgical patients (Achinger et al., 2006). Factors that contribute to hospital-acquired hyponatremia include administration of thiazide diuretics, administration of medications to stimulate ADH, surgery, and overadministration of hypotonic IV fluids (Hoorn et al., 2006). The average duration of an increased length of stay for hospital-acquired hyponatremia is 12 days; therefore it is clear that the condition has a serious impact on health care costs and the patient’s quality of life (Hoorn et al., 2006).

In one study, pediatric oncology patients given hypotonic intravenous fluids were more likely to have hyponatremia with seizures (Duke et al., 2005). Symptomatic hyponatremia and hypoxia have high mortality rates (Kokko, 2006). The mortality rate for acute hyponatremia that develops in less than 48 hours is 50%. In symptomatic hyponatremia, when the serum sodium level is 120 to 130 mEq/L, the mortality rate is 15%. Hyponatremia in early phase ST elevation after an MI is a predictor of long-term mortality (Goldberg et al., 2006).