Hypernatremia in Emergency Medicine
- Author: Zina Semenovskaya, MD; Chief Editor: Romesh Khardori, MD, PhD, FACP more...
Sodium levels are tightly controlled in a healthy individual by regulation of urine concentration and an intact thirst mechanism. Hypernatremia (defined as a serum sodium level >145 mEq/L) is rare in patients with preserved thirst mechanism. When hypernatremia does occur, it is associated with a high mortality rate (>50% in most studies).
Given this high mortality rate, the emergency physician must be able to recognize and treat this condition. This article discusses the patients in whom hypernatremia should be suspected and how to initiate workup and administer appropriate treatment.
In general, hypernatremia can be caused by derangement of the thirst response or altered behavioral response thereto (primarily psychiatric patients, and elderly patients who are institutionalized), impaired renal concentrating mechanism (diabetes insipidus [DI]) secondary to kidney pathology (nephrogenic DI) or difficulty with the neurohormonal control of this concentrating mechanism (central DI), or by losses of free water from other sources.
Assessment and treatment of a hypernatremic patient focuses on 2 important questions:
What is the patient's volume status?
Is the problem acute or chronic?
Water homeostasis is maintained by a balance between water intake and the combined water loss from renal excretion, respiratory, skin, and GI sources. Under normal conditions, water intake and losses are matched. To maintain salt homeostasis, the kidneys similarly adjust urine concentration to match salt intake and loss. See the image below.
Hypernatremia results from disequilibrium of one or both of these balances. Most commonly, the disorder is caused by a relative free water loss, although it can be caused by salt loading. The various ways in which these equilibria can be disturbed are discussed in Causes.
When hypernatremia (of any etiology) occurs, cells become dehydrated. Either the osmotic load of the increased sodium acts to extract water from the cells or a portion of the burden of the body's free water deficit is borne by the cell. (Sodium, primarily an extracellular ion, is actively pumped out of most cells and is the primary determinant of serum osmolarity.) Dehydrated cells shrink from water extraction.
Cells immediately respond to combat this shrinkage and osmotic force by transporting electrolytes across the cell membrane, thus altering rest potentials of electrically active membranes. After an hour of hypernatremia, intracellular organic solutes are generated in an effort to restore cell volume and to avoid structural damage. This protective mechanism is important to remember when treating a patient with hypernatremia. Cerebral edema ensues if water replacement proceeds at a rate that does not allow for excretion or metabolism of accumulated solutes.
The effects of cellular dehydration are seen principally in the CNS, where stretching of shrunken neurons and alteration of membrane potentials from electrolyte flux lead to ineffective functioning. If shrinkage is severe enough, stretching and rupture of bridging veins may cause intracranial hemorrhage.
Hypernatremia occurs in approximately 1% of hospitalized patients. The condition usually develops after hospital admission. An incidence closer to 2% has been reported in debilitated elderly persons and in breastfed infants.[1, 2]
Pediatric patients in developing nations may be at increased risk for hypernatremia because infant feeding may be complicated by poor maternal milk production (secondary to nutritional status) and errors in reconstitution of powdered formula.
The mortality rate from hypernatremia is high, especially among elderly patients. Mortality rates of 42-75% have been reported for acutely evolving hypernatremia and 10-60% for chronic hypernatremia. Because patients with hypernatremia often have other serious comorbidities, precisely evaluating the degree of mortality directly due to hypernatremia is difficult. Morbidity in survivors is high, with many patients experiencing permanent neurologic deficits.
Most deaths are due to an underlying disease process, rather than the hypernatremia itself. Delay in treatment (or inadequate treatment) of hypernatremia increase mortality.
A study by Huang et al indicated that in patients with chronic kidney disease, hypernatremia is associated with an increased risk for all-cause mortality and for deaths unrelated to cardiovascular problems or malignancy. Hyponatremia was found to be associated with an increased risk for the same, as well as for cardiovascular- and malignancy-related mortality. The study included 45,333 patients with stage 3 or 4 chronic kidney disease, 9.2% of whom had dysnatremia.
A Turkish study, by Ates et al, indicated that in patients presenting to emergency departments with severe hypernatremia, independent risk factors for mortality included low systolic blood pressure, low pH, Na+ level over 166 mmol/L, increased plasma osmolarity, a mean sodium reduction rate of -0.134 mmol/L/h or less, dehydration, and, pneumonia. The retrospective study included 256 patients.
In hospitalized patients, persistent hypernatremia and protracted hypotension have been associated with a very poor prognosis.
Hypernatremia is diagnosed in males and females in equal numbers.
Patients who present to the hospital with hypernatremia tend to be at the extremes of age. Breastfed infants occasionally present with hypernatremia in the first weeks of life, and elderly patients who are institutionalized are especially heavily represented.
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