Hypernatremia is defined as a sodium concentration greater than 145 mEq/L. All patients with hypernatremia have hyperosmolality, unlike hyponatremic patients who can have a low, normal, or high serum osmolality. Hypernatremia develops when there is a relative loss of water that is inadequately compensated for by water ingestion. Rarely, administration of excess sodium in relation to water contributes to hypernatremia. This is most often encountered in critically ill patients when large amounts of hypertonic fluid are administered.
The primary responses to hypernatremia are stimulation of thirst (to increase water intake) and increased secretion of ADH (to minimize water loss in the urine). Cells in the hypothalamus can sense minimal changes in serum osmolarity, triggering the thirst mechanism and subsequent intake of water. It is nearly impossible to develop hypernatremia in the context of an intact thirst mechanism with appropriate access to water.
Acute, severe hypernatremia (serum sodium greater than 160 mEq/L) can manifest as lethargy, irritability, and weakness sometimes progressing to hyperthermia, delirium, seizures, and coma. Irreversible neurologic damage may occur if the hypernatremia is left untreated. Because water shifts from the cells to the intravascular space to protect volume status, symptoms may be delayed. Symptoms in older adults may not be specific.
The first steps in evaluating patients with hypernatremia are assessing the urine volume, osmolality, and the osmole excretion rate. The latter can be calculated by multiplying the urine osmolality with urine volume. The copeptin test is discussed below.
The initial step is to determine whether the patient with hypernatremia is oliguric, ie, urine flow less than 0.5 mL/minute, or nonoliguric. Patients who are nonoliguric can be further subdivided by measurement of a urine osmolality.
1. The oliguric patient (urine flow less than 0.5 mL/minute)
This is found in several scenarios.
Hypernatremia will develop in patients with reduced water intake secondary to the inability to communicate and/or limited access to water.
Nonrenal sites of water loss include sweat, GI tract, and the respiratory tract. This is most commonly seen in patients with diarrhea or in febrile patients on a ventilator.
C. SHIFT OF WATER INTO CELLS
Rarely, hypernatremia may manifest from a shift of water into cells due to the intracellular gain of an ...