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Hypernatremia Review PRIMARY CARE Review Articles Primary Care clinical interventions or accidental sodium loading (Table 1 and Fig. 1E). Because sustained hypernatremia can occur only when thirst or access to water is impaired, the groups HYPERNATREMIA at highest risk are patients with altered mental status, intubated patients, infants, and elderly persons.12 Hy- HORACIO J. ADROGUÉ, M.D., pernatremia in infants usually results from diarrhea, AND NICOLAOS E. MADIAS, M.D. whereas in elderly persons it is usually associated with infirmity or febrile illness.6,13,14 Thirst impairment also occurs in elderly patients.15,16 Frail nursing home residents and hospitalized patients are prone to hy- HE serum sodium concentration and thus se- pernatremia because they depend on others for their rum osmolality are closely controlled by wa- water requirements.7 ter homeostasis, which is mediated by thirst, T 1 CLINICAL MANIFESTATIONS arginine vasopressin, and the kidneys. A disruption in the water balance is manifested as an abnormality Signs and symptoms of hypernatremia largely re- in the serum sodium concentration — hypernatre- flect central nervous system dysfunction and are prom- mia or hyponatremia.2,3 Hypernatremia, defined as a inent when the increase in the serum sodium con- rise in the serum sodium concentration to a value ex- centration is large or occurs rapidly (i.e., over a period ceeding 145 mmol per liter, is a common electrolyte of hours).1,6 Most outpatients with hypernatremia disorder. Because sodium is a functionally imperme- are either very young or very old.17 Common symp- able solute, it contributes to tonicity and induces the toms in infants include hyperpnea, muscle weakness, movement of water across cell membranes.4 There- restlessness, a characteristic high-pitched cry, insom- fore, hypernatremia invariably denotes hypertonic hy- nia, lethargy, and even coma.5,13 Convulsions are typ- perosmolality and always causes cellular dehydration, ically absent except in cases of inadvertent sodium at least transiently (Fig. 1). The resultant morbidity loading or aggressive rehydration.14,18,19 Unlike in- may be inconsequential, serious, or even life-threat- fants, elderly patients generally have few symptoms ening.5 Hypernatremia frequently develops in hospi- until the serum sodium concentration exceeds 160 talized patients as an iatrogenic condition, and some mmol per liter.17,20 Intense thirst may be present ini- of its most serious complications result not from the tially, but it dissipates as the disorder progresses and disorder itself but from inappropriate treatment of is absent in patients with hypodipsia.5 The level of it.6,7 In this article, we focus on the management of consciousness is correlated with the severity of the hy- hypernatremia, emphasizing a quantitative approach pernatremia.6 Muscle weakness, confusion, and coma to the correction of the fluid imbalance.8 are sometimes manifestations of coexisting disorders rather than of the hypernatremia itself. CAUSES Unlike hypernatremia in outpatients, hospital- Hypernatremia represents a deficit of water in re- acquired hypernatremia affects patients of all ages.7 lation to the body’s sodium stores, which can result The clinical manifestations are even more elusive in from a net water loss or a hypertonic sodium gain hospitalized patients because they often have preex- (Table 1). Net water loss accounts for the majority isting neurologic dysfunction. As in children, rapid of cases of hypernatremia.9-11 It can occur in the ab- sodium loading in adults can cause convulsions and sence of a sodium deficit (pure water loss) (Fig. 1B) coma.5,21 In patients of all ages, orthostatic hypoten- or in its presence (hypotonic fluid loss) (Fig. 1C and sion and tachycardia reflect marked hypovolemia. 1D). Hypertonic sodium gain usually results from Brain shrinkage induced by hypernatremia can cause vascular rupture, with cerebral bleeding, subarach- noid hemorrhage, and permanent neurologic dam- From the Department of Medicine, Baylor College of Medicine and age or death. Brain shrinkage is countered by an adap- Methodist Hospital, and the Renal Section, Department of Veterans Affairs tive response that is initiated promptly and consists Medical Center, Houston (H.J.A.); and the Department of Medicine, Tufts University School of Medicine, and the Division of Nephrology and Tup- of solute gain by the brain that tends to restore lost per Research Institute, New England Medical Center, Boston (N.E.M.). water. This response leads to the normalization of Address reprint requests to Dr. Madias at the Division of Nephrology, New brain volume and accounts for the milder symptoms England Medical Center, Box 172, 750 Washington St., Boston, MA 22-24 02111, or at [email protected]. of hypernatremia that develops slowly (Fig. 2). ©2000, Massachusetts Medical Society. However, the normalization of brain volume does Volume 342 Number 20 · 1493 Downloaded from www.nejm.org at VA LIBRARY NETWORK on January 24, 2006 . Copyright © 2000 Massachusetts Medical Society. All rights reserved. The New England Journal of Medicine Extracellular Fluid Intracellular Fluid A Normal conditions Hypernatremia due: B to pure water loss: (e.g., from diabetes insipidus) Hypernatremia due: C to hypotonic sodium loss: (e.g., from vomiting) Hypernatremia due: to hypotonic sodium: D and potassium loss: (e.g., from osmotic diuresis) Hypernatremia due: to hypertonic sodium gain: E (e.g., from hypertonic sodium: bicarbonate infusion) Figure 1. Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions and during States of Hyper- natremia. Normally, the extracellular-fluid and intracellular-fluid compartments account for 40 and 60 percent of total body water, respectively (Panel A). Pure water loss reduces the size of each compartment proportionately (Panel B). Contrary to common belief, the volume of extracellular fluid in this setting is reduced, not normal, although the reduction is often not clinically evident. The sodium content of extracellular fluid remains unaltered, yet 1 of each 2.5 liters of water that is lost is from the extracellular-fluid compartment. Hypotonic sodium loss causes a relatively larger loss of volume in the extracellular-fluid compartment than in the intracellular-fluid compartment (Panel C). Potassium loss in addition to hypotonic sodium loss further reduces the intracellular-fluid compartment (Panel D). Hypertonic sodium gain results in an increase in extracellular fluid but a decrease in intracellular fluid (Panel E). In each panel, the open circles denote sodium, and the solid circles potassium; the broken line between the two compartments represents the cell mem- brane, and the shading indicates the intravascular volume. not correct hyperosmolality in the brain. In pa- and correcting the prevailing hypertonicity.3,11 Man- tients with prolonged hyperosmolality, aggressive aging the underlying cause may mean stopping gas- treatment with hypotonic fluids may cause cerebral trointestinal fluid losses; controlling pyrexia, hyper- edema, which can lead to coma, convulsions, and glycemia, and glucosuria; withholding lactulose and death (Fig. 2).14,18,19 diuretics; treating hypercalcemia and hypokalemia; The mortality rate associated with hypernatremia moderating lithium-induced polyuria; or correcting varies widely according to the severity of the condition the feeding preparation. In patients with hypernatre- and the rapidity of its onset. It is difficult, however, to mia that has developed over a period of hours (e.g., separate the contribution of hypernatremia to mortal- those with accidental sodium loading) rapid correc- ity from the contribution of underlying illnesses.11,23 tion improves the prognosis without increasing the risk of cerebral edema, because accumulated electro- MANAGEMENT lytes are rapidly extruded from brain cells.11,22 In such Proper treatment of hypernatremia requires a two- patients, reducing the serum sodium concentration pronged approach: addressing the underlying cause by 1 mmol per liter per hour is appropriate.11 A slow- 1494 · May 18, 2000 Downloaded from www.nejm.org at VA LIBRARY NETWORK on January 24, 2006 . Copyright © 2000 Massachusetts Medical Society. All rights reserved. PRIMARY CARE dition, patients with seizures require prompt anti- TABLE 1. CAUSES OF HYPERNATREMIA. convulsant therapy and adequate ventilation. The preferred route for administering fluids is the Net water loss oral route or a feeding tube; if neither is feasible, flu- Pure water Unreplaced insensible losses (dermal and respiratory) ids should be given intravenously. Only hypotonic Hypodipsia fluids are appropriate, including pure water, 5 percent Neurogenic diabetes insipidus Post-traumatic dextrose, 0.2 percent sodium chloride (referred to as Caused by tumors, cysts, histiocytosis, tuberculosis, one-quarter isotonic saline), and 0.45 percent sodium sarcoidosis chloride (one-half isotonic saline). The more hypoton- Idiopathic Caused by aneurysms, meningitis, encephalitis, ic the infusate, the lower the infusion rate required. Guillain–Barré syndrome Because the risk of cerebral edema increases with the Caused by ethanol ingestion (transient) volume of the infusate, the volume should be re- Congenital nephrogenic diabetes insipidus 25 Acquired nephrogenic diabetes insipidus stricted to that required to correct hypertonicity. Caused by renal disease (e.g., medullary cystic disease) Except in cases of frank circulatory compromise, 0.9 Caused by hypercalcemia or hypokalemia
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