Hypernatremia and Hyponatremia

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13 Hypernatremia and Hyponatremia

Disorders of plasma sodium concentration—that is, hypernatremia and hyponatremia—are among the most common clinical problems observed in the critically ill. These disorders are often asymptomatic, but in some patients, they may result in symptoms ranging from minor to life threatening. The approach to treating hyper- and hyponatremia in individual patients involves balancing the risks of treatment against the risks of the disorder.

image Hypernatremia

Hypernatremia is a common clinical problem, observed in up to 2% of the general hospital population and 15% of patients admitted to the intensive care unit.14 In the outpatient setting, hypernatremia is most prevalent in the geriatric patient population; in hospitalized patients, it is observed in all age groups.1,5 Mortality rates in patients with hypernatremia can range as high as 70%.16 Although the high mortality rate no doubt reflects the severity of underlying disease in these patients, there is significant morbidity related to hypernatremia itself. Neurologic sequelae from hypernatremia are common, particularly in the pediatric population.6

Maintaining a normal serum sodium concentration (135–145 mEq/L) is dependent on the balance between water intake and water excretion. Hypernatremia results from a deficit of free water that leads to an increase in serum tonicity. The usual mechanism underlying the development of hypernatremia is inadequate water intake and increased free water loss, but it can also result from the intake of hypertonic sodium solutions. Hypernatremia may be associated with volume depletion, euvolemia, or hypervolemia, depending on the balance of salt and water loss and intake. Sodium content is low, normal, or high, respectively, in each of these circumstances. Relative sodium and volume status has important implications for the treatment of hypernatremic patients.

The brain is particularly susceptible to the effects of hypernatremia. When the sodium concentration in plasma is higher than normal, water moves across cytosolic membranes (from the inside of cells to the outside of cells) to preserve osmotic equilibrium. As a consequence of intracellular dehydration, there is a net loss of brain volume, which in turn places mechanical stress on cerebral vessels, possibly resulting in bleeding.6 With chronic hypernatremia, however, cellular adaptation occurs. Under these circumstances, so-called idiogenic osmoles accumulate in brain cells, minimizing cellular dehydration. Importantly, the presence of these idiogenic osmoles presents a risk for the development of cerebral edema during the treatment of hypernatremia.

The symptoms of hypernatremia are nonspecific and often difficult to separate from those of underlying illnesses in hospitalized patients. Central nervous system (CNS) abnormalities are most common and can include confusion, weakness, and lethargy in the early stages, progressing to seizures, coma, and death in later stages. The CNS symptoms result from the movement of water out of the brain cells rather than the hypernatremia per se. Neurologic deterioration can be seen during treatment as a result of the development of cerebral edema. Signs of volume depletion or volume overload may be present, depending on the cause of the hypernatremia.

The treatment of hypernatremia is water repletion (Box 13-1). Assuming total body water is 60%, the water deficit may be estimated as follows:


The percentage of water relative to total body weight is actually closer to 50% in women and about 50% in the elderly of both genders. Treatment should be instituted at a rate that balances the risk of hypernatremia with the risk of too rapid correction, particularly in cases of chronic hypernatremia. Half the calculated deficit should be replaced within the first 12 to 24 hours at a rate of sodium concentration correction not over 2 mEq/L per hour. The remainder of the water deficit can be replaced over the next 48 hours. The rapidity of replacement should be determined by the acuteness of onset and severity of symptoms.

Neurologic status has to be closely monitored during replacement for evidence of the development of cerebral edema. Ongoing replacement of fluid and electrolyte losses is also necessary during treatment. In patients with volume depletion and hemodynamic instability associated with hypernatremia, volume replacement with isotonic saline is initially indicated. Once hemodynamic stability is achieved, water replacement can be initiated. Hypotonic saline (e.g., 0.45% saline) may be preferable to water as the replacement fluid for these patients. If hypernatremia is associated with hypervolemia (e.g., as a consequence of treatment with hypertonic saline or hypertonic sodium bicarbonate solution), treatment should be directed toward reducing sodium intake while inducing sodium loss. In these patients, diuretics can be used along with free water (5% dextrose) infusion. Dialysis may be necessary if renal failure is present.