hipernatremia

The serum sodium concentration and thus serum osmolality are closely controlled by water homeostasis, which is mediated by thirst, arginine vasopressin, and the kidneys.1 A disruption in the water balance is manifested as an abnormality in the serum sodium concentration — hypernatremia or hyponatremia.2,3 Hypernatremia, defined as a rise in the serum sodium concentration to a value exceeding 145 mmol per liter, is a common electrolyte disorder. Because sodium is a functionally impermeable solute, it contributes to tonicity and induces the movement of water across cell membranes.4 Therefore, hypernatremia invariably denotes hypertonic hyperosmolality and always causes cellular dehydration, at least transiently (Figure 1Figure 1Extracellular-Fluid and Intracellular-Fluid Compartments under Normal Conditions and during States of Hypernatremia.). The resultant morbidity may be inconsequential, serious, or even life-threatening.5 Hypernatremia frequently develops in hospitalized patients as an iatrogenic condition, and some of its most serious complications result not from the disorder itself but from inappropriate treatment of it.6,7 In this article, we focus on the management of hypernatremia, emphasizing a quantitative approach to the correction of the fluid imbalance.8

Causes

Hypernatremia represents a deficit of water in relation to the body's sodium stores, which can result from a net water loss or a hypertonic sodium gain (Table 1Table 1Causes of Hypernatremia.). Net water loss accounts for the majority of cases of hypernatremia.9-11 It can occur in the absence of a sodium deficit (pure water loss) (Figure 1B) or in its presence (hypotonic fluid loss) (Figure 1C and Figure 1D). Hypertonic sodium gain usually results from clinical interventions or accidental sodium loading (Table 1 and Figure 1E).
Because sustained hypernatremia can occur only when thirst or access to water is impaired, the groups at highest risk are patients with altered mental status, intubated patients, infants, and elderly persons.12 Hypernatremia in infants usually results from diarrhea, 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 hypernatremia because they depend on others for their water requirements.7

Clinical Manifestations

Signs and symptoms of hypernatremia largely reflect central nervous system dysfunction and are prominent when the increase in the serum sodium concentration is large or occurs rapidly (i.e., over a period of hours).1,6 Most outpatients with hypernatremia are either very young or very old.17 Common symptoms in infants include hyperpnea, muscle weakness, restlessness, a characteristic high-pitched cry, insomnia, lethargy, and even coma.5,13 Convulsions are typically absent except in cases of inadvertent sodium loading or aggressive rehydration.14,18,19 Unlike infants, elderly patients generally have few symptoms until the serum sodium concentration exceeds 160 mmol per liter.17,20 Intense thirst may be present initially, but it dissipates as the disorder progresses and is absent in patients with hypodipsia.5 The level of consciousness is correlated with the severity of the hypernatremia.6 Muscle weakness, confusion, and coma are sometimes manifestations of coexisting disorders rather than of the hypernatremia itself.
Unlike hypernatremia in outpatients, hospital-acquired hypernatremia affects patients of all ages.7 The clinical manifestations are even more elusive in hospitalized patients because they often have preexisting neurologic dysfunction. As in children, rapid sodium loading in adults can cause convulsions and coma.5,21 In patients of all ages, orthostatic hypotension and tachycardia reflect marked hypovolemia.
Brain shrinkage induced by hypernatremia can cause vascular rupture, with cerebral bleeding, subarachnoid hemorrhage, and permanent neurologic damage or death. Brain shrinkage is countered by an adaptive response that is initiated promptly and consists of solute gain by the brain that tends to restore lost water. This response leads to the normalization of brain volume and accounts for the milder symptoms of hypernatremia that develops slowly (Figure 2Figure 2Effects of Hypernatremia on the Brain and Adaptive Responses.).22-24 However, the normalization of brain volume does not correct hyperosmolality in the brain. In patients with prolonged hyperosmolality, aggressive treatment with hypotonic fluids may cause cerebral edema, which can lead to coma, convulsions, and death (Figure 2).14,18,19
The mortality rate associated with hypernatremia varies widely according to the severity of the condition and the rapidity of its onset. It is difficult, however, to separate the contribution of hypernatremia to mortality from the contribution of underlying illnesses.11,23


http://www.nejm.org/doi/pdf/10.1056/NEJM200005183422006